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\n  \n 2021\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Characteristics and progression of patients with frontotemporal dementia in a regional memory clinic network.\n \n \n \n\n\n \n Leroy, M.; Bertoux, M.; Skrobala, E.; Mode, E.; Adnet-Bonte, C.; Le Ber, I.; Bombois, S.; Cassagnaud, P.; Chen, Y.; Deramecourt, V.; Lebert, F.; Mackowiak, M. A.; Sillaire, A. R.; Wathelet, M.; Pasquier, F.; Lebouvier, T.; and Méotis network\n\n\n \n\n\n\n Alzheimer's Research & Therapy, 13(1): 19. January 2021.\n \n\n\n\n
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@article{leroy_characteristics_2021,\n\ttitle = {Characteristics and progression of patients with frontotemporal dementia in a regional memory clinic network},\n\tvolume = {13},\n\tissn = {1758-9193},\n\tdoi = {10.1186/s13195-020-00753-9},\n\tabstract = {BACKGROUND: Due to heterogeneous clinical presentation, difficult differential diagnosis with Alzheimer's disease (AD) and psychiatric disorders, and evolving clinical criteria, the epidemiology and natural history of frontotemporal lobar degeneration (FTD) remain elusive. In order to better characterize FTD patients, we relied on the database of a regional memory clinic network with standardized diagnostic procedures and chose AD patients as a comparator.\nMETHODS: Patients that were first referred to our network between January 2010 and December 2016 and whose last clinical diagnosis was degenerative or vascular dementia were included. Comparisons were conducted between FTD and AD as well as between the different FTD syndromes, divided into language variants (lvFTD), behavioral variant (bvFTD), and FTD with primarily motor symptoms (mFTD). Cognitive progression was estimated with the yearly decline in Mini Mental State Examination (MMSE).\nRESULTS: Among the patients that were referred to our network in the 6-year time span, 690 were ultimately diagnosed with FTD and 18,831 with AD. Patients with FTD syndromes represented 2.6\\% of all-cause dementias. The age-standardized incidence was 2.90 per 100,000 person-year and incidence peaked between 75 and 79 years. Compared to AD, patients with FTD syndromes had a longer referral delay and delay to diagnosis. Patients with FTD syndromes had a higher MMSE score than AD at first referral while their progression was similar. mFTD patients had the shortest survival while survival in bvFTD, lvFTD, and AD did not significantly differ. FTD patients, especially those with the behavioral variant, received more antidepressants, anxiolytics, and antipsychotics than AD patients.\nCONCLUSIONS: FTD syndromes differ with AD in characteristics at baseline, progression rate, and treatment. Despite a broad use of the new diagnostic criteria in an organized memory clinic network, FTD syndromes are longer to diagnose and account for a low proportion of dementia cases, suggesting persistent underdiagnosis. Congruent with recent publications, the late peak of incidence warns against considering FTD as being exclusively a young-onset dementia.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Alzheimer's Research \\& Therapy},\n\tauthor = {Leroy, Mélanie and Bertoux, Maxime and Skrobala, Emilie and Mode, Elisa and Adnet-Bonte, Catherine and Le Ber, Isabelle and Bombois, Stéphanie and Cassagnaud, Pascaline and Chen, Yaohua and Deramecourt, Vincent and Lebert, Florence and Mackowiak, Marie Anne and Sillaire, Adeline Rollin and Wathelet, Marielle and Pasquier, Florence and Lebouvier, Thibaud and {Méotis network}},\n\tmonth = jan,\n\tyear = {2021},\n\tpmid = {33419472},\n\tpmcid = {PMC7796569},\n\tkeywords = {Dementia, Epidemiology, Frontotemporal dementia, Progression},\n\tpages = {19},\n}\n\n
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\n BACKGROUND: Due to heterogeneous clinical presentation, difficult differential diagnosis with Alzheimer's disease (AD) and psychiatric disorders, and evolving clinical criteria, the epidemiology and natural history of frontotemporal lobar degeneration (FTD) remain elusive. In order to better characterize FTD patients, we relied on the database of a regional memory clinic network with standardized diagnostic procedures and chose AD patients as a comparator. METHODS: Patients that were first referred to our network between January 2010 and December 2016 and whose last clinical diagnosis was degenerative or vascular dementia were included. Comparisons were conducted between FTD and AD as well as between the different FTD syndromes, divided into language variants (lvFTD), behavioral variant (bvFTD), and FTD with primarily motor symptoms (mFTD). Cognitive progression was estimated with the yearly decline in Mini Mental State Examination (MMSE). RESULTS: Among the patients that were referred to our network in the 6-year time span, 690 were ultimately diagnosed with FTD and 18,831 with AD. Patients with FTD syndromes represented 2.6% of all-cause dementias. The age-standardized incidence was 2.90 per 100,000 person-year and incidence peaked between 75 and 79 years. Compared to AD, patients with FTD syndromes had a longer referral delay and delay to diagnosis. Patients with FTD syndromes had a higher MMSE score than AD at first referral while their progression was similar. mFTD patients had the shortest survival while survival in bvFTD, lvFTD, and AD did not significantly differ. FTD patients, especially those with the behavioral variant, received more antidepressants, anxiolytics, and antipsychotics than AD patients. CONCLUSIONS: FTD syndromes differ with AD in characteristics at baseline, progression rate, and treatment. Despite a broad use of the new diagnostic criteria in an organized memory clinic network, FTD syndromes are longer to diagnose and account for a low proportion of dementia cases, suggesting persistent underdiagnosis. Congruent with recent publications, the late peak of incidence warns against considering FTD as being exclusively a young-onset dementia.\n
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\n \n\n \n \n \n \n \n Defining brain health: A concept analysis.\n \n \n \n\n\n \n Chen, Y.; Demnitz, N.; Yamamoto, S.; Yaffe, K.; Lawlor, B.; and Leroi, I.\n\n\n \n\n\n\n International Journal of Geriatric Psychiatry. April 2021.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{chen_defining_2021,\n\ttitle = {Defining brain health: {A} concept analysis},\n\tissn = {1099-1166},\n\tshorttitle = {Defining brain health},\n\tdoi = {10.1002/gps.5564},\n\tabstract = {OBJECTIVES: Brain health is an important focus for coming decades due to population ageing. Although the term 'brain health' is increasingly used in lay and professional settings, a clear definition of the term is lacking. We conducted an analysis of the concept of brain health to inform policy, practice, and research.\nMETHODS: We applied a hybrid concept analysis method involving three stages: (1) a review of the extant literature for definitions of brain health; (2) field work, involving an international survey of 'brain health' researchers and practitioners; and (3) a final analysis, integrating the findings into a working definition and model.\nRESULTS: Our review of the literature identified 13 articles defining brain health, six of which proposed their own definition. Our survey revealed that the term 'brain health' was used in diverse ways based on different theoretical frameworks. From the review and survey, we extracted attributes, antecedents, and consequences of brain health. These were synthesized into a definition of brain health as a life-long, multidimensional, dynamic state consisting of cognitive, emotional and motor domains underpinned by physiological processes and can be objectively measured and subjectively experienced. It is influenced by eco-biopsychosocial determinants.\nCONCLUSION: This working definition of brain health is a foundation for developing policy, practice, research and advocacy. The definition needs to be operationalised through further development of empirical referents, including cross-cultural understanding, adaptation and validation.},\n\tlanguage = {eng},\n\tjournal = {International Journal of Geriatric Psychiatry},\n\tauthor = {Chen, Yaohua and Demnitz, Naiara and Yamamoto, Stacey and Yaffe, Kristine and Lawlor, Brian and Leroi, Iracema},\n\tmonth = apr,\n\tyear = {2021},\n\tpmid = {34131954},\n\tkeywords = {brain health, brain resilience, cognitive reserve, concept analysis, concept map, definition, dementia, dementia prevention, mental health},\n}\n
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\n OBJECTIVES: Brain health is an important focus for coming decades due to population ageing. Although the term 'brain health' is increasingly used in lay and professional settings, a clear definition of the term is lacking. We conducted an analysis of the concept of brain health to inform policy, practice, and research. METHODS: We applied a hybrid concept analysis method involving three stages: (1) a review of the extant literature for definitions of brain health; (2) field work, involving an international survey of 'brain health' researchers and practitioners; and (3) a final analysis, integrating the findings into a working definition and model. RESULTS: Our review of the literature identified 13 articles defining brain health, six of which proposed their own definition. Our survey revealed that the term 'brain health' was used in diverse ways based on different theoretical frameworks. From the review and survey, we extracted attributes, antecedents, and consequences of brain health. These were synthesized into a definition of brain health as a life-long, multidimensional, dynamic state consisting of cognitive, emotional and motor domains underpinned by physiological processes and can be objectively measured and subjectively experienced. It is influenced by eco-biopsychosocial determinants. CONCLUSION: This working definition of brain health is a foundation for developing policy, practice, research and advocacy. The definition needs to be operationalised through further development of empirical referents, including cross-cultural understanding, adaptation and validation.\n
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\n  \n 2020\n \n \n (9)\n \n \n
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\n \n\n \n \n \n \n \n Twenty-year trends in patient referrals throughout the creation and development of a regional memory clinic network.\n \n \n \n\n\n \n Chen, Y.; Lebouvier, T.; Skrobala, E.; Volpe-Gillot, L.; Huvent-Grelle, D.; Jourdan, N.; Leroy, M.; Richard, F.; Pasquier, F.; ; and the Meotis network \n\n\n \n\n\n\n Alzheimer's & Dementia (New York, N. Y.), 6(1): e12048. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{chen_twenty-year_2020,\n\ttitle = {Twenty-year trends in patient referrals throughout the creation and development of a regional memory clinic network},\n\tvolume = {6},\n\tissn = {2352-8737},\n\tdoi = {10.1002/trc2.12048},\n\tabstract = {Introduction: Memory clinics (MCs) are the main model for dementia diagnosis and care. Following the development of a MC network in Northern France, our objectives were to assess its impact on patient characteristics over 20 years.\nMethods: The characteristics of new consultants were studied from 1997 to 2016.\nResults: New consultants increased from 774 per year in 1997 to 26258 per year in 2016, as the number of MCs increased from 12 to 29. Over time, patients were progressively older and less educated, and more were living alone. A greater proportion of patients were referred by specialists. Referral delay and home-to-MC distance kept decreasing. The oldest patients were referred at a progressively less-severe stage. The proportion of young patients kept increasing in the tertiary referral center.\nDiscussions: The development of a region-wide MC network led to increased referral of vulnerable patients and differentiation of the tertiary referral center over time.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Alzheimer's \\& Dementia (New York, N. Y.)},\n\tauthor = {Chen, Yaohua and Lebouvier, Thibaud and Skrobala, Emilie and Volpe-Gillot, Lisette and Huvent-Grelle, Dominique and Jourdan, Nathalie and Leroy, Mélanie and Richard, Florence and Pasquier, Florence and {and the Meotis network}},\n\tyear = {2020},\n\tpmid = {32875059},\n\tpmcid = {PMC7449245},\n\tkeywords = {Alzheimer's disease, ambulatory care facilities, community, dementia, health networks, memory clinics, public health practice, public health, public health policies},\n\tpages = {e12048},\n}\n\n
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\n Introduction: Memory clinics (MCs) are the main model for dementia diagnosis and care. Following the development of a MC network in Northern France, our objectives were to assess its impact on patient characteristics over 20 years. Methods: The characteristics of new consultants were studied from 1997 to 2016. Results: New consultants increased from 774 per year in 1997 to 26258 per year in 2016, as the number of MCs increased from 12 to 29. Over time, patients were progressively older and less educated, and more were living alone. A greater proportion of patients were referred by specialists. Referral delay and home-to-MC distance kept decreasing. The oldest patients were referred at a progressively less-severe stage. The proportion of young patients kept increasing in the tertiary referral center. Discussions: The development of a region-wide MC network led to increased referral of vulnerable patients and differentiation of the tertiary referral center over time.\n
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\n \n\n \n \n \n \n \n Diagnosis of severe cognitive disorder: the family history as a key issue.\n \n \n \n\n\n \n Derollez, C.; Haik, S.; Pasquier, F.; De Toffol, B.; and Bombois, S.\n\n\n \n\n\n\n Neurological Sciences: Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 41(7): 1945–1947. July 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{derollez_diagnosis_2020,\n\ttitle = {Diagnosis of severe cognitive disorder: the family history as a key issue},\n\tvolume = {41},\n\tissn = {1590-3478},\n\tshorttitle = {Diagnosis of severe cognitive disorder},\n\tdoi = {10.1007/s10072-019-04226-2},\n\tlanguage = {eng},\n\tnumber = {7},\n\tjournal = {Neurological Sciences: Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology},\n\tauthor = {Derollez, Céline and Haik, Stéphane and Pasquier, Florence and De Toffol, Bertrand and Bombois, Stéphanie},\n\tmonth = jul,\n\tyear = {2020},\n\tpmid = {31965421},\n\tpages = {1945--1947},\n}\n\n
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\n \n\n \n \n \n \n \n The Clinical Value of the Faux Pas Test for Diagnosing Behavioral-Variant Frontotemporal Dementia.\n \n \n \n\n\n \n Delbeuck, X.; Pollet, M.; Pasquier, F.; Bombois, S.; and Moroni, C.\n\n\n \n\n\n\n Journal of Geriatric Psychiatry and Neurology,891988720964253. October 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{delbeuck_clinical_2020,\n\ttitle = {The {Clinical} {Value} of the {Faux} {Pas} {Test} for {Diagnosing} {Behavioral}-{Variant} {Frontotemporal} {Dementia}},\n\tissn = {0891-9887},\n\tdoi = {10.1177/0891988720964253},\n\tabstract = {OBJECTIVE: We studied the clinical value of the faux pas test to diagnose behavioral-variant frontotemporal dementia.\nMETHODS: The faux pas test was administered to patients referred to a memory clinic in a context of behavioral disturbances. The diagnosis of behavioral-variant frontotemporal dementia (n = 14) or not (n = 25) was confirmed after a 3 years follow-up.\nRESULTS: The faux pas test displayed a high sensitivity for behavioral-variant frontotemporal dementia (.83) however its specificity was only moderate (.64).\nCONCLUSIONS: Our results confirm that the FPT capture's specific cognitive impairments in patients with behavioral-variant frontotemporal dementia. However, some patients with psychiatric disease or other neurological diseases may also show impaired scores.},\n\tlanguage = {eng},\n\tjournal = {Journal of Geriatric Psychiatry and Neurology},\n\tauthor = {Delbeuck, Xavier and Pollet, Marianne and Pasquier, Florence and Bombois, Stéphanie and Moroni, Christine},\n\tmonth = oct,\n\tyear = {2020},\n\tpmid = {33030088},\n\tkeywords = {behavioral symptoms, bipolar disorder, differential diagnosis, frontotemporal dementia, social cognition, theory of mind},\n\tpages = {891988720964253},\n}\n\n
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\n OBJECTIVE: We studied the clinical value of the faux pas test to diagnose behavioral-variant frontotemporal dementia. METHODS: The faux pas test was administered to patients referred to a memory clinic in a context of behavioral disturbances. The diagnosis of behavioral-variant frontotemporal dementia (n = 14) or not (n = 25) was confirmed after a 3 years follow-up. RESULTS: The faux pas test displayed a high sensitivity for behavioral-variant frontotemporal dementia (.83) however its specificity was only moderate (.64). CONCLUSIONS: Our results confirm that the FPT capture's specific cognitive impairments in patients with behavioral-variant frontotemporal dementia. However, some patients with psychiatric disease or other neurological diseases may also show impaired scores.\n
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\n \n\n \n \n \n \n \n Does amnesia specifically predict Alzheimer's pathology? A neuropathological study.\n \n \n \n\n\n \n Bertoux, M.; Cassagnaud, P.; Lebouvier, T.; Lebert, F.; Sarazin, M.; Le Ber, I.; Dubois, B.; NeuroCEB Brain Bank; Auriacombe, S.; Hannequin, D.; Wallon, D.; Ceccaldi, M.; Maurage, C.; Deramecourt, V.; and Pasquier, F.\n\n\n \n\n\n\n Neurobiology of Aging, 95: 123–130. November 2020.\n \n\n\n\n
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@article{bertoux_does_2020,\n\ttitle = {Does amnesia specifically predict {Alzheimer}'s pathology? {A} neuropathological study},\n\tvolume = {95},\n\tissn = {1558-1497},\n\tshorttitle = {Does amnesia specifically predict {Alzheimer}'s pathology?},\n\tdoi = {10.1016/j.neurobiolaging.2020.07.011},\n\tabstract = {Amnesia is a key component of Alzheimer's disease (AD) and the most important feature of its clinical diagnosis but its specificity has recently been challenged. This study investigated the ability of amnesia to predict AD in a clinicopathological dementia series. Ninety-one patients to which free and cued verbal memory assessment was administered during early cognitive decline, were followed until autopsy. Patients' histological diagnoses were classified as pure AD, mixed AD, and non-AD pathologies. Data-driven automated classification procedures explored the correspondence between memory performance and pathological diagnoses. Classifications revealed 3 clusters of performance reflecting different levels of amnesia. Little correspondence between these clusters and the presence of AD pathology was retrieved. A third of patients with pure/mixed AD pathology were non-amnesic at presentation and ≈45\\% of patients without AD pathology were amnesic. Data-driven prediction of AD pathology based on memory also had a poor accuracy. Free and cued memory assessments are fair tools to diagnose an amnesic syndrome but lack accuracy to predict AD pathology.},\n\tlanguage = {eng},\n\tjournal = {Neurobiology of Aging},\n\tauthor = {Bertoux, Maxime and Cassagnaud, Pascaline and Lebouvier, Thibaud and Lebert, Florence and Sarazin, Marie and Le Ber, Isabelle and Dubois, Bruno and {NeuroCEB Brain Bank} and Auriacombe, Sophie and Hannequin, Didier and Wallon, David and Ceccaldi, Mathieu and Maurage, Claude-Alain and Deramecourt, Vincent and Pasquier, Florence},\n\tmonth = nov,\n\tyear = {2020},\n\tpmid = {32795849},\n\tkeywords = {AD pathology, Alzheimer’s disease, Amnesia, FCSRT, Free and cued, Memory},\n\tpages = {123--130},\n}\n\n
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\n Amnesia is a key component of Alzheimer's disease (AD) and the most important feature of its clinical diagnosis but its specificity has recently been challenged. This study investigated the ability of amnesia to predict AD in a clinicopathological dementia series. Ninety-one patients to which free and cued verbal memory assessment was administered during early cognitive decline, were followed until autopsy. Patients' histological diagnoses were classified as pure AD, mixed AD, and non-AD pathologies. Data-driven automated classification procedures explored the correspondence between memory performance and pathological diagnoses. Classifications revealed 3 clusters of performance reflecting different levels of amnesia. Little correspondence between these clusters and the presence of AD pathology was retrieved. A third of patients with pure/mixed AD pathology were non-amnesic at presentation and ≈45% of patients without AD pathology were amnesic. Data-driven prediction of AD pathology based on memory also had a poor accuracy. Free and cued memory assessments are fair tools to diagnose an amnesic syndrome but lack accuracy to predict AD pathology.\n
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\n \n\n \n \n \n \n \n The Influence of Baseline Alzheimer's Disease Severity on Cognitive Decline and CSF Biomarkers in the NILVAD Trial.\n \n \n \n\n\n \n Abdullah, L.; Crawford, F.; Tsolaki, M.; Börjesson-Hanson, A.; Olde Rikkert, M.; Pasquier, F.; Wallin, A.; Kennelly, S.; Ait-Ghezala, G.; Paris, D.; Hendrix, S.; Blennow, K.; Lawlor, B.; and Mullan, M.\n\n\n \n\n\n\n Frontiers in Neurology, 11: 149. 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{abdullah_influence_2020,\n\ttitle = {The {Influence} of {Baseline} {Alzheimer}'s {Disease} {Severity} on {Cognitive} {Decline} and {CSF} {Biomarkers} in the {NILVAD} {Trial}},\n\tvolume = {11},\n\tissn = {1664-2295},\n\tdoi = {10.3389/fneur.2020.00149},\n\tabstract = {We examined the effects of a dihydropyridine calcium channel blocker nilvadipine with anti-inflammatory properties on cognition and cerebrospinal fluid (CSF) biomarkers by baseline Alzheimer's disease (AD) severity. Exploratory analyses were performed on the dataset (n = 497) of a phase III randomized placebo-controlled trial to examine the response to nilvadipine in AD subjects stratified by baseline AD severity into very mild (MMSE ≥ 25), mild (MMSE 20-24) and moderate AD (MMSE {\\textless} 20). The outcome measures included total and subscale scores of the Alzheimer's Disease Assessment Scale Cognitive 12 (ADAS-Cog 12), the Clinical Dementia Rating Scale sum of boxes (CDR-sb) and the AD composite score (ADCOMS). Cerebrospinal fluid biomarkers Aβ38, Aβ40, Aβ42, neurofilament light chain (NFL), neurogranin, YKL-40, total tau and P181 tau (ptau) were measured in a subset of samples (n = 55). Regression analyses were adjusted for confounders to specifically examine the influence of nilvadipine and baseline AD severity on cognitive outcomes over 78-weeks. Compared to their respective placebo-controls, nilvadipine-treated, very mild AD subjects showed less decline, whereas moderate AD subjects showed a greater cognitive decline on the ADAS-Cog 12 test and the ADCOMS. A lower decline was observed after nilvadipine treatment for a composite memory trait in very mild AD subjects and a composite language trait in mild AD subjects. Cerebrospinal fluid Aβ42/Aβ40 ratios were increased in mild AD and decreased in moderate AD patients treated with nilvadipine, compared to their respective controls. Among moderate AD subjects, levels of ptau, total tau, neurogranin and YKL-40 increased in subjects treated with nilvadipine compared to placebo. These studies suggest that baseline AD severity influenced the treatment outcome in the NILVAD trial and that future clinical trials of nilvadipine should be restricted to mild and very mild AD patients. Trial Registration: NCT02017340 Registered 20 December 2013, https://clinicaltrials.gov/ct2/show/NCT02017340 EUDRACT Reference Number 2012-002764-27 Registered 04 February 2013, https://www.clinicaltrialsregister.eu/ctr-search/search?query=2012-002764-27.},\n\tlanguage = {eng},\n\tjournal = {Frontiers in Neurology},\n\tauthor = {Abdullah, Laila and Crawford, Fiona and Tsolaki, Magda and Börjesson-Hanson, Anne and Olde Rikkert, Marcel and Pasquier, Florence and Wallin, Anders and Kennelly, Sean and Ait-Ghezala, Ghania and Paris, Daniel and Hendrix, Suzanne and Blennow, Kaj and Lawlor, Brian and Mullan, Michael},\n\tyear = {2020},\n\tpmid = {32210906},\n\tpmcid = {PMC7067750},\n\tkeywords = {cerebrospinal fluid Aβ42/Aβ40 ratios, cognitive decline, exploratory analysis, mild Alzheimer's disease, nilvadipine},\n\tpages = {149},\n}\n\n
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\n We examined the effects of a dihydropyridine calcium channel blocker nilvadipine with anti-inflammatory properties on cognition and cerebrospinal fluid (CSF) biomarkers by baseline Alzheimer's disease (AD) severity. Exploratory analyses were performed on the dataset (n = 497) of a phase III randomized placebo-controlled trial to examine the response to nilvadipine in AD subjects stratified by baseline AD severity into very mild (MMSE ≥ 25), mild (MMSE 20-24) and moderate AD (MMSE \\textless 20). The outcome measures included total and subscale scores of the Alzheimer's Disease Assessment Scale Cognitive 12 (ADAS-Cog 12), the Clinical Dementia Rating Scale sum of boxes (CDR-sb) and the AD composite score (ADCOMS). Cerebrospinal fluid biomarkers Aβ38, Aβ40, Aβ42, neurofilament light chain (NFL), neurogranin, YKL-40, total tau and P181 tau (ptau) were measured in a subset of samples (n = 55). Regression analyses were adjusted for confounders to specifically examine the influence of nilvadipine and baseline AD severity on cognitive outcomes over 78-weeks. Compared to their respective placebo-controls, nilvadipine-treated, very mild AD subjects showed less decline, whereas moderate AD subjects showed a greater cognitive decline on the ADAS-Cog 12 test and the ADCOMS. A lower decline was observed after nilvadipine treatment for a composite memory trait in very mild AD subjects and a composite language trait in mild AD subjects. Cerebrospinal fluid Aβ42/Aβ40 ratios were increased in mild AD and decreased in moderate AD patients treated with nilvadipine, compared to their respective controls. Among moderate AD subjects, levels of ptau, total tau, neurogranin and YKL-40 increased in subjects treated with nilvadipine compared to placebo. These studies suggest that baseline AD severity influenced the treatment outcome in the NILVAD trial and that future clinical trials of nilvadipine should be restricted to mild and very mild AD patients. Trial Registration: NCT02017340 Registered 20 December 2013, https://clinicaltrials.gov/ct2/show/NCT02017340 EUDRACT Reference Number 2012-002764-27 Registered 04 February 2013, https://www.clinicaltrialsregister.eu/ctr-search/search?query=2012-002764-27.\n
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\n \n\n \n \n \n \n \n Antihypertensive agents in Alzheimer's disease: beyond vascular protection.\n \n \n \n\n\n \n Lebouvier, T.; Chen, Y.; Duriez, P.; Pasquier, F.; and Bordet, R.\n\n\n \n\n\n\n Expert Review of Neurotherapeutics, 20(2): 175–187. February 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{lebouvier_antihypertensive_2020,\n\ttitle = {Antihypertensive agents in {Alzheimer}'s disease: beyond vascular protection},\n\tvolume = {20},\n\tissn = {1744-8360},\n\tshorttitle = {Antihypertensive agents in {Alzheimer}'s disease},\n\tdoi = {10.1080/14737175.2020.1708195},\n\tabstract = {Introduction: Midlife hypertension has been consistently linked with increased risk of cognitive decline and Alzheimer's disease (AD). Observational studies and randomized trials show that the use of antihypertensive therapy is associated with a lesser incidence or prevalence of cognitive impairment and dementia. However, whether antihypertensive agents specifically target the pathological process of AD remains elusive.Areas covered: This review of literature provides an update on the clinical and preclinical arguments supporting anti-AD properties of antihypertensive drugs. The authors focused on validated all classes of antihypertensive treatments such as angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), calcium channel blockers (CCB), β-blockers, diuretics, neprilysin inhibitors, and other agents. Three main mechanisms can be advocated: action on the concurrent vascular pathology, action on the vascular component of Alzheimer's pathophysiology, and action on nonvascular targets.Expert opinion: In 2019, while there is no doubt that hypertension should be treated in primary prevention of vascular disease and in secondary prevention of stroke and mixed dementia, the place of antihypertensive agents in the secondary prevention of 'pure' AD remains an outstanding question.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Expert Review of Neurotherapeutics},\n\tauthor = {Lebouvier, Thibaud and Chen, Yaohua and Duriez, Patrick and Pasquier, Florence and Bordet, Régis},\n\tmonth = feb,\n\tyear = {2020},\n\tpmid = {31869274},\n\tkeywords = {Alzheimer Disease, Alzheimer’s disease, Antihypertensive Agents, Humans, Secondary Prevention, antihypertensive agents, hypertension, neuroprotection, pathology, prevention, treatment, vascular risk factors},\n\tpages = {175--187},\n}\n\n
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\n Introduction: Midlife hypertension has been consistently linked with increased risk of cognitive decline and Alzheimer's disease (AD). Observational studies and randomized trials show that the use of antihypertensive therapy is associated with a lesser incidence or prevalence of cognitive impairment and dementia. However, whether antihypertensive agents specifically target the pathological process of AD remains elusive.Areas covered: This review of literature provides an update on the clinical and preclinical arguments supporting anti-AD properties of antihypertensive drugs. The authors focused on validated all classes of antihypertensive treatments such as angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), calcium channel blockers (CCB), β-blockers, diuretics, neprilysin inhibitors, and other agents. Three main mechanisms can be advocated: action on the concurrent vascular pathology, action on the vascular component of Alzheimer's pathophysiology, and action on nonvascular targets.Expert opinion: In 2019, while there is no doubt that hypertension should be treated in primary prevention of vascular disease and in secondary prevention of stroke and mixed dementia, the place of antihypertensive agents in the secondary prevention of 'pure' AD remains an outstanding question.\n
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\n \n\n \n \n \n \n \n What the COVID-19 pandemic entails for the management of patients with behavioral and psychological symptoms of dementia: experience in France.\n \n \n \n\n\n \n Drunat, O.; Roche, J.; Kohler, S.; Julien, V.; Pascal, S.; Lenoir, H.; Soto-Martin, M.; Lepetit, A.; Volpe-Gillot, L.; Leclercq, V.; Romdhani, M.; Koskas, P.; and Lebert, F.\n\n\n \n\n\n\n International Psychogeriatrics, 32(11): 1361–1364. November 2020.\n \n\n\n\n
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@article{drunat_what_2020,\n\ttitle = {What the {COVID}-19 pandemic entails for the management of patients with behavioral and psychological symptoms of dementia: experience in {France}},\n\tvolume = {32},\n\tissn = {1741-203X},\n\tshorttitle = {What the {COVID}-19 pandemic entails for the management of patients with behavioral and psychological symptoms of dementia},\n\tdoi = {10.1017/S1041610220003567},\n\tlanguage = {eng},\n\tnumber = {11},\n\tjournal = {International Psychogeriatrics},\n\tauthor = {Drunat, Olivier and Roche, Jean and Kohler, Samuel and Julien, Vernaudon and Pascal, Saidlitz and Lenoir, Hermine and Soto-Martin, Maria and Lepetit, Alexis and Volpe-Gillot, Lisette and Leclercq, Vania and Romdhani, Mouna and Koskas, Pierre and Lebert, Florence},\n\tmonth = nov,\n\tyear = {2020},\n\tpmid = {32930087},\n\tpmcid = {PMC7573453},\n\tkeywords = {Aged, Aged, 80 and over, COVID-19, Dementia, Disease Outbreaks, France, Humans, Pandemics, Patient Care Management, Practice Guidelines as Topic, Problem Behavior, SARS-CoV-2},\n\tpages = {1361--1364},\n}\n\n
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\n \n\n \n \n \n \n \n Normal ageing of the brain: Histological and biological aspects.\n \n \n \n\n\n \n Teissier, T.; Boulanger, E.; and Deramecourt, V.\n\n\n \n\n\n\n Revue Neurologique, 176(9): 649–660. November 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{teissier_normal_2020,\n\ttitle = {Normal ageing of the brain: {Histological} and biological aspects},\n\tvolume = {176},\n\tissn = {0035-3787},\n\tshorttitle = {Normal ageing of the brain},\n\tdoi = {10.1016/j.neurol.2020.03.017},\n\tabstract = {All the hallmarks of ageing are observed in the brain, and its cells, especially neurons, are characterized by their remarkably long lifetime. Like any organ or system, the brain is exposed to ageing processes which affect molecules, cells, blood vessels, gross morphology and, uniquely for this organ, cognition. The preponderant cerebral structures are characterized by the cellular processes of neurons and glial cells and while the quantity of cerebral interstitial fluid is limited, it is now recognized as playing a crucial role in maintaining cerebral homeostasis. Most of our current knowledge of the ageing brain derives from studies of neurodegenerative disorders. It is interesting to note that common features of these disorders, like Tau, phosphoTau and amyloid peptide accumulation, can begin relatively early in life as a result of physiological ageing and are present in subclinical cases while also being used as early-stage markers of neurodegenerative diseases in progression. In this article, we review tissue and cellular modifications in the ageing brain. Commonly described macroscopic, microscopic and vascular changes that in the ageing brain are contrasted with those seen in neurodegenerative contexts. We also review the molecular changes that occur with age in the brain, such as modifications in gene expression, insulin/insulin-like growth factor 1 signalling dysfunction, post-translational protein modifications, mitochondrial dysfunction, autophagy and calcium conductance changes.},\n\tlanguage = {eng},\n\tnumber = {9},\n\tjournal = {Revue Neurologique},\n\tauthor = {Teissier, T. and Boulanger, E. and Deramecourt, V.},\n\tmonth = nov,\n\tyear = {2020},\n\tpmid = {32418702},\n\tpages = {649--660},\n}\n\n
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\n All the hallmarks of ageing are observed in the brain, and its cells, especially neurons, are characterized by their remarkably long lifetime. Like any organ or system, the brain is exposed to ageing processes which affect molecules, cells, blood vessels, gross morphology and, uniquely for this organ, cognition. The preponderant cerebral structures are characterized by the cellular processes of neurons and glial cells and while the quantity of cerebral interstitial fluid is limited, it is now recognized as playing a crucial role in maintaining cerebral homeostasis. Most of our current knowledge of the ageing brain derives from studies of neurodegenerative disorders. It is interesting to note that common features of these disorders, like Tau, phosphoTau and amyloid peptide accumulation, can begin relatively early in life as a result of physiological ageing and are present in subclinical cases while also being used as early-stage markers of neurodegenerative diseases in progression. In this article, we review tissue and cellular modifications in the ageing brain. Commonly described macroscopic, microscopic and vascular changes that in the ageing brain are contrasted with those seen in neurodegenerative contexts. We also review the molecular changes that occur with age in the brain, such as modifications in gene expression, insulin/insulin-like growth factor 1 signalling dysfunction, post-translational protein modifications, mitochondrial dysfunction, autophagy and calcium conductance changes.\n
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\n \n\n \n \n \n \n \n \n When affect overlaps with concept: emotion recognition in semantic variant of primary progressive aphasia.\n \n \n \n \n\n\n \n Bertoux, M.; Duclos, H.; Caillaud, M.; Segobin, S.; Merck, C.; de La Sayette, V.; Belliard, S.; Desgranges, B.; Eustache, F.; and Laisney, M.\n\n\n \n\n\n\n Brain, 143(12): 3850–3864. December 2020.\n \n\n\n\n
\n\n\n\n \n \n \"WhenPaper\n  \n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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@article{bertoux_when_2020,\n\ttitle = {When affect overlaps with concept: emotion recognition in semantic variant of primary progressive aphasia},\n\tvolume = {143},\n\tissn = {0006-8950, 1460-2156},\n\tshorttitle = {When affect overlaps with concept},\n\turl = {https://academic.oup.com/brain/article/143/12/3850/5998326},\n\tdoi = {10.1093/brain/awaa313},\n\tabstract = {Abstract\n            The most recent theories of emotions have postulated that their expression and recognition depend on acquired conceptual knowledge. In other words, the conceptual knowledge derived from prior experiences guide our ability to make sense of such emotions. However, clear evidence is still lacking to contradict more traditional theories, considering emotions as innate, distinct and universal physiological states. In addition, whether valence processing (i.e. recognition of the pleasant/unpleasant character of emotions) also relies on semantic knowledge is yet to be determined. To investigate the contribution of semantic knowledge to facial emotion recognition and valence processing, we conducted a behavioural and neuroimaging study in 20 controls and 16 patients with the semantic variant of primary progressive aphasia, a neurodegenerative disease that is prototypical of semantic memory impairment, and in which an emotion recognition deficit has already been described. We assessed participants’ knowledge of emotion concepts and recognition of 10 basic (e.g. anger) or self-conscious (e.g. embarrassment) facial emotional expressions presented both statically (images) and dynamically (videos). All participants also underwent a brain MRI. Group comparisons revealed deficits in both emotion concept knowledge and emotion recognition in patients, independently of type of emotion and presentation. These measures were significantly correlated with each other in patients and with semantic fluency in patients and controls. Neuroimaging analyses showed that both emotion recognition and emotion conceptual knowledge were correlated with reduced grey matter density in similar areas within frontal ventral, temporal, insular and striatal regions, together with white fibre degeneration in tracts connecting frontal regions with each other as well as with temporal regions. We then performed a qualitative analysis of responses made during the facial emotion recognition task, by delineating valence errors (when one emotion was mistaken for another of a different valence), from other errors made during the emotion recognition test. We found that patients made more valence errors. The number of valence errors correlated with emotion conceptual knowledge as well as with reduced grey matter volume in brain regions already retrieved to correlate with this score. Specificity analyses allowed us to conclude that this cognitive relationship and anatomical overlap were not mediated by a general effect of disease severity. Our findings suggest that semantic knowledge guides the recognition of emotions and is also involved in valence processing. Our study supports a constructionist view of emotion recognition and valence processing, and could help to refine current theories on the interweaving of semantic knowledge and emotion processing.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2021-02-10},\n\tjournal = {Brain},\n\tauthor = {Bertoux, Maxime and Duclos, Harmony and Caillaud, Marie and Segobin, Shailendra and Merck, Catherine and de La Sayette, Vincent and Belliard, Serge and Desgranges, Béatrice and Eustache, Francis and Laisney, Mickaël},\n\tmonth = dec,\n\tyear = {2020},\n\tpages = {3850--3864},\n}\n\n
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\n Abstract The most recent theories of emotions have postulated that their expression and recognition depend on acquired conceptual knowledge. In other words, the conceptual knowledge derived from prior experiences guide our ability to make sense of such emotions. However, clear evidence is still lacking to contradict more traditional theories, considering emotions as innate, distinct and universal physiological states. In addition, whether valence processing (i.e. recognition of the pleasant/unpleasant character of emotions) also relies on semantic knowledge is yet to be determined. To investigate the contribution of semantic knowledge to facial emotion recognition and valence processing, we conducted a behavioural and neuroimaging study in 20 controls and 16 patients with the semantic variant of primary progressive aphasia, a neurodegenerative disease that is prototypical of semantic memory impairment, and in which an emotion recognition deficit has already been described. We assessed participants’ knowledge of emotion concepts and recognition of 10 basic (e.g. anger) or self-conscious (e.g. embarrassment) facial emotional expressions presented both statically (images) and dynamically (videos). All participants also underwent a brain MRI. Group comparisons revealed deficits in both emotion concept knowledge and emotion recognition in patients, independently of type of emotion and presentation. These measures were significantly correlated with each other in patients and with semantic fluency in patients and controls. Neuroimaging analyses showed that both emotion recognition and emotion conceptual knowledge were correlated with reduced grey matter density in similar areas within frontal ventral, temporal, insular and striatal regions, together with white fibre degeneration in tracts connecting frontal regions with each other as well as with temporal regions. We then performed a qualitative analysis of responses made during the facial emotion recognition task, by delineating valence errors (when one emotion was mistaken for another of a different valence), from other errors made during the emotion recognition test. We found that patients made more valence errors. The number of valence errors correlated with emotion conceptual knowledge as well as with reduced grey matter volume in brain regions already retrieved to correlate with this score. Specificity analyses allowed us to conclude that this cognitive relationship and anatomical overlap were not mediated by a general effect of disease severity. Our findings suggest that semantic knowledge guides the recognition of emotions and is also involved in valence processing. Our study supports a constructionist view of emotion recognition and valence processing, and could help to refine current theories on the interweaving of semantic knowledge and emotion processing.\n
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\n  \n 2019\n \n \n (3)\n \n \n
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\n \n\n \n \n \n \n \n Is endoscopic third ventriculostomy safe and efficient in the treatment of obstructive chronic hydrocephalus in adults? A prospective clinical and MRI study.\n \n \n \n\n\n \n Baroncini, M.; Kuchcinski, G.; Le Thuc, V.; Bourgeois, P.; Leroy, H. A.; Baille, G.; Lebouvier, T.; and Defebvre, L.\n\n\n \n\n\n\n Acta Neurochirurgica, 161(7): 1353–1360. July 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{baroncini_is_2019,\n\ttitle = {Is endoscopic third ventriculostomy safe and efficient in the treatment of obstructive chronic hydrocephalus in adults? {A} prospective clinical and {MRI} study},\n\tvolume = {161},\n\tissn = {0942-0940},\n\tshorttitle = {Is endoscopic third ventriculostomy safe and efficient in the treatment of obstructive chronic hydrocephalus in adults?},\n\tdoi = {10.1007/s00701-019-03932-2},\n\tabstract = {BACKGROUND: In case of suspected normal pressure hydrocephalus, MRI is performed systematically and can sometimes highlight an obstruction of the flow pathways of the CSF (aqueductal stenosis or other downstream obstruction). It seems legitimate for these patients to ask the question of a treatment with endoscopic third ventriculostomy (ETV), even if the late decompensation of an obstruction may suggest an association with a CSF resorption disorder. The aim of this study was to evaluate clinical and radiological evolution after ETV in a group of elderly patients with an obstructive chronic hydrocephalus (OCH).\nMETHODS: ETV was performed in 15 patients with OCH between 2012 and 2017. Morphometric (callosal angle, ventricular surface, third ventricular width, and Evans' index) and velocimetric parameters (stroke volume of the aqueductal (SVa) CSF) parameters were measured prior and after surgery with brain MRI. The clinical score (mini-mental status examination (MMSE) and the modified Larsson's score, evaluating walking, autonomy, and incontinence) were performed pre- and postoperatively.\nRESULTS: SVa was less than 15 μL/R-R in 12 out of the 15 patients; in the other three cases, the obstruction was located at a distance from the middle part of the aqueduct. Fourteen out of 15 patients were significantly improved: mean Larsson's score decreased from 3.8 to 0.6 (P ≤ 0.01) and mean MMSE increased from 25.7 to 28 (P = 0.084). Evans' index and ventricular area decreased postoperatively and the callosal angle increased (P ≤ 0.01). The mean follow-up lasted 17.9 months. No postoperative complications were observed.\nCONCLUSION: ETV seems to be a safe and efficient alternative to shunt for chronic hydrocephalus with obstruction; the clinical improvement is usual and ventricular size decreases slightly.},\n\tlanguage = {eng},\n\tnumber = {7},\n\tjournal = {Acta Neurochirurgica},\n\tauthor = {Baroncini, Marc and Kuchcinski, Gregory and Le Thuc, Vianney and Bourgeois, Philippe and Leroy, Henri Arthur and Baille, Guillaume and Lebouvier, Thibaud and Defebvre, Luc},\n\tmonth = jul,\n\tyear = {2019},\n\tpmid = {31069530},\n\tkeywords = {Aged, Aqueductal stenosis, Chronic hydrocephalus, Endoscopy, Female, Humans, Hydrocephalus, MRI, Magnetic Resonance Imaging, Male, Normal pressure hydrocephalus, Postoperative Complications, Third Ventricle, Third ventricle, Ventriculostomy},\n\tpages = {1353--1360},\n}\n\n
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\n BACKGROUND: In case of suspected normal pressure hydrocephalus, MRI is performed systematically and can sometimes highlight an obstruction of the flow pathways of the CSF (aqueductal stenosis or other downstream obstruction). It seems legitimate for these patients to ask the question of a treatment with endoscopic third ventriculostomy (ETV), even if the late decompensation of an obstruction may suggest an association with a CSF resorption disorder. The aim of this study was to evaluate clinical and radiological evolution after ETV in a group of elderly patients with an obstructive chronic hydrocephalus (OCH). METHODS: ETV was performed in 15 patients with OCH between 2012 and 2017. Morphometric (callosal angle, ventricular surface, third ventricular width, and Evans' index) and velocimetric parameters (stroke volume of the aqueductal (SVa) CSF) parameters were measured prior and after surgery with brain MRI. The clinical score (mini-mental status examination (MMSE) and the modified Larsson's score, evaluating walking, autonomy, and incontinence) were performed pre- and postoperatively. RESULTS: SVa was less than 15 μL/R-R in 12 out of the 15 patients; in the other three cases, the obstruction was located at a distance from the middle part of the aqueduct. Fourteen out of 15 patients were significantly improved: mean Larsson's score decreased from 3.8 to 0.6 (P ≤ 0.01) and mean MMSE increased from 25.7 to 28 (P = 0.084). Evans' index and ventricular area decreased postoperatively and the callosal angle increased (P ≤ 0.01). The mean follow-up lasted 17.9 months. No postoperative complications were observed. CONCLUSION: ETV seems to be a safe and efficient alternative to shunt for chronic hydrocephalus with obstruction; the clinical improvement is usual and ventricular size decreases slightly.\n
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\n \n\n \n \n \n \n \n Frontotemporal dementia is the leading cause of \"true\" A-/T+ profiles defined with Aβ42/40 ratio.\n \n \n \n\n\n \n Pouclet-Courtemanche, H.; Nguyen, T.; Skrobala, E.; Boutoleau-Bretonnière, C.; Pasquier, F.; Bouaziz-Amar, E.; Bigot-Corbel, E.; Schraen, S.; Dumurgier, J.; Paquet, C.; and Lebouvier, T.\n\n\n \n\n\n\n Alzheimer's & Dementia (Amsterdam, Netherlands), 11: 161–169. December 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pouclet-courtemanche_frontotemporal_2019,\n\ttitle = {Frontotemporal dementia is the leading cause of "true" {A}-/{T}+ profiles defined with {Aβ42}/40 ratio},\n\tvolume = {11},\n\tissn = {2352-8729},\n\tdoi = {10.1016/j.dadm.2019.01.001},\n\tabstract = {Introduction: Patients with positive tauopathy but negative Aβ42 (A-T+) in the cerebrospinal fluid (CSF) represent a diagnostic challenge. The Aβ42/40 ratio supersedes Aβ42 and reintegrates "false" A-T+ patients into the Alzheimer's disease spectrum. However, the biomarker and clinical characteristics of "true" and "false" A-T+ patients remain elusive.\nMethods: Among the 509 T+N+ patients extracted from the databases of three memory clinics, we analyzed T+N+ patients with normal Aβ42 and compared "false" A-T+ with abnormal Aβ42/40 ratio and "true" A-T+ patients with normal Aβ42/40 ratio, before CSF analysis and at follow-up.\nResults: 24.9\\% of T+N+ patients had normal Aβ42 levels. Among them, 42.7\\% were "true" A-T+. "True" A-T+ had lower CSF tauP181 than "false" A-T+ patients. 48.0\\% of "true" A-T+ patients were diagnosed with frontotemporal lobar degeneration before CSF analysis and 64.0\\% at follow-up, as compared with 6\\% in the "false" A-T+ group (P {\\textless} .0001).\nDiscussion: Frontotemporal lobar degeneration is probably the main cause of "true" A-T+ profiles.},\n\tlanguage = {eng},\n\tjournal = {Alzheimer's \\& Dementia (Amsterdam, Netherlands)},\n\tauthor = {Pouclet-Courtemanche, Hélène and Nguyen, Tri-Bao and Skrobala, Emilie and Boutoleau-Bretonnière, Claire and Pasquier, Florence and Bouaziz-Amar, Elodie and Bigot-Corbel, Edith and Schraen, Susanna and Dumurgier, Julien and Paquet, Claire and Lebouvier, Thibaud},\n\tmonth = dec,\n\tyear = {2019},\n\tpmid = {30815533},\n\tpmcid = {PMC6378630},\n\tkeywords = {Alzheimer's disease, Aβ42/40 ratio, Aβ42/Aβ40 ratio, Cerebrospinal fluid biomarkers, Frontotemporal dementia, Suspected non Alzheimer's disease pathology (SNAP)},\n\tpages = {161--169},\n}\n\n
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\n Introduction: Patients with positive tauopathy but negative Aβ42 (A-T+) in the cerebrospinal fluid (CSF) represent a diagnostic challenge. The Aβ42/40 ratio supersedes Aβ42 and reintegrates \"false\" A-T+ patients into the Alzheimer's disease spectrum. However, the biomarker and clinical characteristics of \"true\" and \"false\" A-T+ patients remain elusive. Methods: Among the 509 T+N+ patients extracted from the databases of three memory clinics, we analyzed T+N+ patients with normal Aβ42 and compared \"false\" A-T+ with abnormal Aβ42/40 ratio and \"true\" A-T+ patients with normal Aβ42/40 ratio, before CSF analysis and at follow-up. Results: 24.9% of T+N+ patients had normal Aβ42 levels. Among them, 42.7% were \"true\" A-T+. \"True\" A-T+ had lower CSF tauP181 than \"false\" A-T+ patients. 48.0% of \"true\" A-T+ patients were diagnosed with frontotemporal lobar degeneration before CSF analysis and 64.0% at follow-up, as compared with 6% in the \"false\" A-T+ group (P \\textless .0001). Discussion: Frontotemporal lobar degeneration is probably the main cause of \"true\" A-T+ profiles.\n
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\n \n\n \n \n \n \n \n [The French memory clinics network system].\n \n \n \n\n\n \n Rachez, C.; Desprez, A.; Hertzog, M.; Bruniaux, P.; Adnet, C.; and Pasquier, F.\n\n\n \n\n\n\n Geriatrie Et Psychologie Neuropsychiatrie Du Vieillissement, 17(4): 429–437. December 2019.\n \n\n\n\n
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@article{rachez_french_2019,\n\ttitle = {[{The} {French} memory clinics network system]},\n\tvolume = {17},\n\tissn = {2115-7863},\n\tdoi = {10.1684/pnv.2019.0831},\n\tabstract = {In France, the management of patients with neurocognitive disorders is based on a network of memory clinics. The current operating mode is presented with projects aiming to its improvement, and potential evolution. Interviews were conducted at Memory resources and research centers (CMRR) as well as at the Regional health authorities (ARS) on organization, difficulties, innovation and projects for care management of patients suffering from Alzheimer's disease or related disorder. Twenty-seven semi-structured interviews were performed at the CMRR, and ten with the ARS. The collaboration with the medico-social and associative sectors was unequal. All CMRR were involved in clinical research. The links between ARS and CMRR were sometimes difficult with a lack of dialogue on the projects. However, many innovative plans have been led by the memory clinics and have sometimes been supported by the Health authorities: a therapeutic education program for patients with mild cognitive disorders, deployment of tele-medicine consultations to diagnose neurocognitive disorders in nursing home residents, setting of a network for management of behavioral disorders, creation of a mobile team specialized in clinical research, and creation of a multidisciplinary consultation following diagnosis to work on a personalized care plan. Experienced professionals mentioned a mature and efficient structure of the care management system thanks to the CMRRs' labeling and the different Alzheimer's national plans. However, this highly specialized system does not meet the demands of integrated care and should adapt to the increasing prevalence of patients. Therefore, structuration of primary care should be an emerging subject of reflection at national and international level.},\n\tlanguage = {fre},\n\tnumber = {4},\n\tjournal = {Geriatrie Et Psychologie Neuropsychiatrie Du Vieillissement},\n\tauthor = {Rachez, Chloé and Desprez, Anne and Hertzog, Maurice and Bruniaux, Philippe and Adnet, Catherine and Pasquier, Florence},\n\tmonth = dec,\n\tyear = {2019},\n\tpmid = {31848129},\n\tkeywords = {Aged, Alheimer's disease, Alzheimer Disease, France, Humans, Mental Health Services, Neurocognitive Disorders, associated disorders, care management, memory clinics},\n\tpages = {429--437},\n}\n\n
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\n In France, the management of patients with neurocognitive disorders is based on a network of memory clinics. The current operating mode is presented with projects aiming to its improvement, and potential evolution. Interviews were conducted at Memory resources and research centers (CMRR) as well as at the Regional health authorities (ARS) on organization, difficulties, innovation and projects for care management of patients suffering from Alzheimer's disease or related disorder. Twenty-seven semi-structured interviews were performed at the CMRR, and ten with the ARS. The collaboration with the medico-social and associative sectors was unequal. All CMRR were involved in clinical research. The links between ARS and CMRR were sometimes difficult with a lack of dialogue on the projects. However, many innovative plans have been led by the memory clinics and have sometimes been supported by the Health authorities: a therapeutic education program for patients with mild cognitive disorders, deployment of tele-medicine consultations to diagnose neurocognitive disorders in nursing home residents, setting of a network for management of behavioral disorders, creation of a mobile team specialized in clinical research, and creation of a multidisciplinary consultation following diagnosis to work on a personalized care plan. Experienced professionals mentioned a mature and efficient structure of the care management system thanks to the CMRRs' labeling and the different Alzheimer's national plans. However, this highly specialized system does not meet the demands of integrated care and should adapt to the increasing prevalence of patients. Therefore, structuration of primary care should be an emerging subject of reflection at national and international level.\n
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\n  \n 2018\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Influence of Lewy Pathology on Alzheimer's Disease Phenotype: A Retrospective Clinico-Pathological Study.\n \n \n \n\n\n \n Roudil, J.; Deramecourt, V.; Dufournet, B.; Dubois, B.; Ceccaldi, M.; Duyckaerts, C.; Pasquier, F.; Lebouvier, T.; and Brainbank Neuro-CEB Neuropathology Network\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 63(4): 1317–1323. 2018.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{roudil_influence_2018,\n\ttitle = {Influence of {Lewy} {Pathology} on {Alzheimer}'s {Disease} {Phenotype}: {A} {Retrospective} {Clinico}-{Pathological} {Study}},\n\tvolume = {63},\n\tissn = {1875-8908},\n\tshorttitle = {Influence of {Lewy} {Pathology} on {Alzheimer}'s {Disease} {Phenotype}},\n\tdoi = {10.3233/JAD-170914},\n\tabstract = {BACKGROUND: Studies have shown the frequent coexistence of Lewy pathology (LP) in Alzheimer's Disease (AD).\nOBJECTIVE: The aim of this study was to determine the influence of LP on the clinical and cognitive phenotype in a cohort of patients with a neuropathological diagnosis of AD.\nMETHODS: We reviewed neuropathologically proven AD cases, reaching Braak stages V and VI in the brain banks of Lille and Paris between 1993 and 2016, and classified them according to LP extension (amygdala, brainstem, limbic, or neocortical). We then searched patient files for all available clinical and neuropsychiatric features and neuropsychological data.\nRESULTS: Thirty-three subjects were selected for this study, among which 16 were devoid of LP and 17 presented AD with concomitant LP. The latter were stratified into two subgroups according to LP distribution: 7 were AD with amygdala LP and 10 were AD with 'classical' (brainstem, limbic or neocortical) LP. When analyzing the incidence of each clinical feature at any point during the disease course, we found no significant difference in symptom frequency between the three groups. However, fluctuations appeared significantly earlier in patients with classical LP (2±3.5 years) than in patients without LP (7±1.7 years) or with amygdala LP (8±2.8 years; p {\\textless} 0.01). There was no significant difference in cognitive profiles.\nCONCLUSION: Our findings suggest that the influence of LP on the clinical phenotype of AD is subtle. Core features of dementia with Lewy bodies do not allow clinical diagnosis of a concomitant LP on a patient-to-patient basis.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Roudil, Jennifer and Deramecourt, Vincent and Dufournet, Boris and Dubois, Bruno and Ceccaldi, Mathieu and Duyckaerts, Charles and Pasquier, Florence and Lebouvier, Thibaud and {Brainbank Neuro-CEB Neuropathology Network}},\n\tyear = {2018},\n\tpmid = {29758938},\n\tpmcid = {PMC6218122},\n\tkeywords = {Aged, Alzheimer Disease, Alzheimer’s disease, Alzheimer’s disease with amygdala Lewy bodies, Amygdala, Autopsy, Cognition Disorders, Female, Humans, Lewy Body Disease, Lewy bodies, Lewy body variant of Alzheimer’s disease, Male, Middle Aged, Neuropsychological Tests, Psychiatric Status Rating Scales, Retrospective Studies, braak \nstages, dementia with Lewy bodies, neurofibrillary tangles},\n\tpages = {1317--1323},\n}\n\n
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\n BACKGROUND: Studies have shown the frequent coexistence of Lewy pathology (LP) in Alzheimer's Disease (AD). OBJECTIVE: The aim of this study was to determine the influence of LP on the clinical and cognitive phenotype in a cohort of patients with a neuropathological diagnosis of AD. METHODS: We reviewed neuropathologically proven AD cases, reaching Braak stages V and VI in the brain banks of Lille and Paris between 1993 and 2016, and classified them according to LP extension (amygdala, brainstem, limbic, or neocortical). We then searched patient files for all available clinical and neuropsychiatric features and neuropsychological data. RESULTS: Thirty-three subjects were selected for this study, among which 16 were devoid of LP and 17 presented AD with concomitant LP. The latter were stratified into two subgroups according to LP distribution: 7 were AD with amygdala LP and 10 were AD with 'classical' (brainstem, limbic or neocortical) LP. When analyzing the incidence of each clinical feature at any point during the disease course, we found no significant difference in symptom frequency between the three groups. However, fluctuations appeared significantly earlier in patients with classical LP (2±3.5 years) than in patients without LP (7±1.7 years) or with amygdala LP (8±2.8 years; p \\textless 0.01). There was no significant difference in cognitive profiles. CONCLUSION: Our findings suggest that the influence of LP on the clinical phenotype of AD is subtle. Core features of dementia with Lewy bodies do not allow clinical diagnosis of a concomitant LP on a patient-to-patient basis.\n
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\n \n\n \n \n \n \n \n Relevance of Follow-Up in Patients with Core Clinical Criteria for Alzheimer Disease and Normal CSF Biomarkers.\n \n \n \n\n\n \n Vercruysse, O.; Paquet, C.; Gabelle, A.; Delbeuck, X.; Blanc, F.; Wallon, D.; Dumurgier, J.; Magnin, E.; Martinaud, O.; Jung, B.; Bousiges, O.; Lehmann, S.; Delaby, C.; Quillard-Murain, M.; Peoc H, K.; Laplanche, J.; Bouaziz-Amar, E.; Hannequin, D.; Sablonniere, B.; Buee, L.; Hugon, J.; Schraen, S.; Pasquier, F.; Bombois, S.; and For The E-Plm Group, n.\n\n\n \n\n\n\n Current Alzheimer Research, 15(7): 691–700. 2018.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{vercruysse_relevance_2018,\n\ttitle = {Relevance of {Follow}-{Up} in {Patients} with {Core} {Clinical} {Criteria} for {Alzheimer} {Disease} and {Normal} {CSF} {Biomarkers}},\n\tvolume = {15},\n\tissn = {1875-5828},\n\tdoi = {10.2174/1567205015666180110113238},\n\tabstract = {BACKGROUND: Few patients with a normal cerebrospinal fluid (CSF) biomarker profile fulfill the clinical criteria for Alzheimer disease (AD).\nOBJECTIVE: The aim of this study was to test the hypothesis of misdiagnoses for these patients.\nMETHOD: Patients from the e-PLM centers fulfilling the core clinical criteria for probable AD dementia or mild cognitive impairment due to AD (AD-MCI), with normal CSF Aβ1-42, T-tau and P-tau biomarkers and clinical follow-up, were included. Clinical and imaging data were reviewed by an independent board, from baseline (visit with clinical evaluation and CSF analysis) to the end of the follow-up, for a final diagnosis.\nRESULTS: In the e-PLM cohort of 1098 AD patients with CSF analysis, 37 (3.3\\%) patients (20 with AD dementia core clinical criteria and 17 with AD-MCI core clinical criteria) had normal CSF biomarker profile and a clinical follow-up. All patients presented with episodic memory impairment and 27 (73\\%) had medial temporal lobe atrophy on MRI-scan. After a median follow-up of 36 months (range 7-74), the final diagnosis was AD MCI or dementia for 9 (24\\%) patients, and unlikely due to AD for 28 (76\\%) patients. A misdiagnosis was corrected in 18 (49\\%) patients (mood disorders, non-AD degenerative dementia, vascular cognitive impairment, alcohol cognitive disorders, temporal epilepsy and hippocampal sclerosis), and 10 (27\\%) patients had cognitive disorders of undetermined etiology.\nCONCLUSION: AD diagnosis (MCI or dementia) with normal CSF biomarkers is a rare condition. A clinical follow- up is particularly recommended to consider an alternative diagnosis.},\n\tlanguage = {eng},\n\tnumber = {7},\n\tjournal = {Current Alzheimer Research},\n\tauthor = {Vercruysse, Olivier and Paquet, Claire and Gabelle, Audrey and Delbeuck, Xavier and Blanc, Frederic and Wallon, David and Dumurgier, Julien and Magnin, Eloi and Martinaud, Olivier and Jung, Barbara and Bousiges, Olivier and Lehmann, Sylvain and Delaby, Constance and Quillard-Murain, Muriel and Peoc H, Katell and Laplanche, Jean-Louis and Bouaziz-Amar, Elodie and Hannequin, Didier and Sablonniere, Bernard and Buee, Luc and Hugon, Jacques and Schraen, Susanna and Pasquier, Florence and Bombois, Stephanie and For The E-Plm Group, null},\n\tyear = {2018},\n\tpmid = {29318973},\n\tkeywords = {Aged, Alzheimer Disease, Alzheimer disease, Amyloid beta-Peptides, Biomarkers, Brain, Cognitive Dysfunction, Diagnosis, Differential, Diagnostic Errors, Female, Follow-Up Studies, Humans, Male, Peptide Fragments, Phosphorylation, Retrospective Studies, biomarker, cerebrospinal fluid, dementia, depression, frontotemporal\ndementia, mild cognitive impairment, tau Proteins, vascular dementia.},\n\tpages = {691--700},\n}\n\n
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\n BACKGROUND: Few patients with a normal cerebrospinal fluid (CSF) biomarker profile fulfill the clinical criteria for Alzheimer disease (AD). OBJECTIVE: The aim of this study was to test the hypothesis of misdiagnoses for these patients. METHOD: Patients from the e-PLM centers fulfilling the core clinical criteria for probable AD dementia or mild cognitive impairment due to AD (AD-MCI), with normal CSF Aβ1-42, T-tau and P-tau biomarkers and clinical follow-up, were included. Clinical and imaging data were reviewed by an independent board, from baseline (visit with clinical evaluation and CSF analysis) to the end of the follow-up, for a final diagnosis. RESULTS: In the e-PLM cohort of 1098 AD patients with CSF analysis, 37 (3.3%) patients (20 with AD dementia core clinical criteria and 17 with AD-MCI core clinical criteria) had normal CSF biomarker profile and a clinical follow-up. All patients presented with episodic memory impairment and 27 (73%) had medial temporal lobe atrophy on MRI-scan. After a median follow-up of 36 months (range 7-74), the final diagnosis was AD MCI or dementia for 9 (24%) patients, and unlikely due to AD for 28 (76%) patients. A misdiagnosis was corrected in 18 (49%) patients (mood disorders, non-AD degenerative dementia, vascular cognitive impairment, alcohol cognitive disorders, temporal epilepsy and hippocampal sclerosis), and 10 (27%) patients had cognitive disorders of undetermined etiology. CONCLUSION: AD diagnosis (MCI or dementia) with normal CSF biomarkers is a rare condition. A clinical follow- up is particularly recommended to consider an alternative diagnosis.\n
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\n  \n 2017\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Low Prevalence and Clinical Effect of Vascular Risk Factors in Early-Onset Alzheimer's Disease.\n \n \n \n\n\n \n Chen, Y.; Sillaire, A. R.; Dallongeville, J.; Skrobala, E.; Wallon, D.; Dubois, B.; Hannequin, D.; Pasquier, F.; and Lille YOD study group\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 60(3): 1045–1054. 2017.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{chen_low_2017,\n\ttitle = {Low {Prevalence} and {Clinical} {Effect} of {Vascular} {Risk} {Factors} in {Early}-{Onset} {Alzheimer}'s {Disease}},\n\tvolume = {60},\n\tissn = {1875-8908},\n\tdoi = {10.3233/JAD-170367},\n\tabstract = {BACKGROUND: Determinants of early-onset Alzheimer's disease (EOAD) are not well known. In late-onset AD, vascular risk factors (VRFs) are associated with earlier clinical manifestation.\nOBJECTIVE: The objective of this study was to assess the putative association between VRFs and EOAD.\nMETHODS: We studied participants with dementia meeting criteria for EOAD (recruited into the French CoMAJ prospective cohort study from 1 June 2009 to 28 February 2014) and age-, gender-matched controls (ratio 1:3, drawn randomly from the French MONA-LISA population-based survey between 2005 and 2007). Demographic data, VRFs, comorbidities, treatments, and APOE genotypes were compared in multivariable logistic regression analyses.\nRESULTS: We studied 102 participants with dementia (mean±standard deviation age: 59.5±3.8; women: 59.8\\%) and 306 controls. Compared with controls, EOAD participants had spent less time in formal education (9.9±2.9 versus 11.7±3.8 y; p {\\textless} 0.0001), were less likely to be regular alcohol consumers (p {\\textless} 0.0001), had a lower body mass index (-2 kg/m2; p {\\textless} 0.0004), and a lower mean systolic blood pressure (-6.2 mmHg; p = 0.0036). The prevalence of APOE ɛ4 allele was higher in participants with dementia than in controls (50\\% versus 29.4\\%; p = 0.0002), as was the prevalence of depression (48\\% versus 32\\%; p {\\textless} 0.001). Similar results were observed in multivariable analysis. Compared with EOAD participants lacking VRFs, EOAD participants with at least one VRF had a higher prevalence of depression (29.6\\% versus 53.3\\%, respectively; p = 0.03).\nCONCLUSION: The prevalence of VRFs is not elevated in EOAD patients (in contrast to older AD patients). Extensive genetic testing should be considered more frequently in the context of EOAD.},\n\tlanguage = {eng},\n\tnumber = {3},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Chen, Yaohua and Sillaire, Adeline Rollin and Dallongeville, Jean and Skrobala, Emilie and Wallon, David and Dubois, Bruno and Hannequin, Didier and Pasquier, Florence and {Lille YOD study group}},\n\tyear = {2017},\n\tpmid = {28984595},\n\tpmcid = {PMC5676853},\n\tkeywords = {APOE, Age of Onset, Alzheimer Disease, Animals, Apolipoproteins E, Cardiovascular Diseases, Comorbidity, Female, France, Humans, Logistic Models, Longitudinal Studies, Male, Middle Aged, Multivariate Analysis, Prevalence, Prospective Studies, Risk Factors, early onset Alzheimer disease, late onset Alzheimer disease, vascular \nrisk factors},\n\tpages = {1045--1054},\n}\n\n
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\n BACKGROUND: Determinants of early-onset Alzheimer's disease (EOAD) are not well known. In late-onset AD, vascular risk factors (VRFs) are associated with earlier clinical manifestation. OBJECTIVE: The objective of this study was to assess the putative association between VRFs and EOAD. METHODS: We studied participants with dementia meeting criteria for EOAD (recruited into the French CoMAJ prospective cohort study from 1 June 2009 to 28 February 2014) and age-, gender-matched controls (ratio 1:3, drawn randomly from the French MONA-LISA population-based survey between 2005 and 2007). Demographic data, VRFs, comorbidities, treatments, and APOE genotypes were compared in multivariable logistic regression analyses. RESULTS: We studied 102 participants with dementia (mean±standard deviation age: 59.5±3.8; women: 59.8%) and 306 controls. Compared with controls, EOAD participants had spent less time in formal education (9.9±2.9 versus 11.7±3.8 y; p \\textless 0.0001), were less likely to be regular alcohol consumers (p \\textless 0.0001), had a lower body mass index (-2 kg/m2; p \\textless 0.0004), and a lower mean systolic blood pressure (-6.2 mmHg; p = 0.0036). The prevalence of APOE ɛ4 allele was higher in participants with dementia than in controls (50% versus 29.4%; p = 0.0002), as was the prevalence of depression (48% versus 32%; p \\textless 0.001). Similar results were observed in multivariable analysis. Compared with EOAD participants lacking VRFs, EOAD participants with at least one VRF had a higher prevalence of depression (29.6% versus 53.3%, respectively; p = 0.03). CONCLUSION: The prevalence of VRFs is not elevated in EOAD patients (in contrast to older AD patients). Extensive genetic testing should be considered more frequently in the context of EOAD.\n
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\n \n\n \n \n \n \n \n Update on tauopathies.\n \n \n \n\n\n \n Lebouvier, T.; Pasquier, F.; and Buée, L.\n\n\n \n\n\n\n Current Opinion in Neurology, 30(6): 589–598. December 2017.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{lebouvier_update_2017,\n\ttitle = {Update on tauopathies},\n\tvolume = {30},\n\tissn = {1473-6551},\n\tdoi = {10.1097/WCO.0000000000000502},\n\tabstract = {PURPOSE OF REVIEW: The purpose of this review is to provide an update on the role of tau beyond the stabilization of microtubules and on the clinical, pathological, diagnostic and therapeutic aspects of tauopathies.\nRECENT FINDINGS: Beyond its function as a microtubule-associated tau protein, tau is also involved in gene regulation, signal transduction and metabolism. Experimental models allow for the development of new diagnostic and therapeutic tools. Tauopathies encompass different disorders that may manifest with various clinical syndromes. Differential diagnosis with other proteinopathies is still challenging. Cerebrospinal fluid biomarkers and radiotracers were extensively studied in the last year. Although diagnostic accuracy remains deceiving in non-Alzheimer's disease tauopathies, positron emission tomography tau tracers could be used to monitor disease progression.\nSUMMARY: Despite the advent of novel therapeutic approaches and the increasing number of clinical trials in tauopathies, accurate clinical diagnosis is still an unmet need and better tau biomarkers are still desperately needed. Although primary taupathies are rare and heterogeneous disorders, their combined prevalence and the importance of tau disorder in Alzheimer's disease and secondary tauopathies makes research on tauopathy a priority - because it could benefit many patients.},\n\tlanguage = {eng},\n\tnumber = {6},\n\tjournal = {Current Opinion in Neurology},\n\tauthor = {Lebouvier, Thibaud and Pasquier, Florence and Buée, Luc},\n\tmonth = dec,\n\tyear = {2017},\n\tpmid = {28914736},\n\tkeywords = {Animals, Dementia, Humans, Tauopathies, tau Proteins},\n\tpages = {589--598},\n}\n\n
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\n PURPOSE OF REVIEW: The purpose of this review is to provide an update on the role of tau beyond the stabilization of microtubules and on the clinical, pathological, diagnostic and therapeutic aspects of tauopathies. RECENT FINDINGS: Beyond its function as a microtubule-associated tau protein, tau is also involved in gene regulation, signal transduction and metabolism. Experimental models allow for the development of new diagnostic and therapeutic tools. Tauopathies encompass different disorders that may manifest with various clinical syndromes. Differential diagnosis with other proteinopathies is still challenging. Cerebrospinal fluid biomarkers and radiotracers were extensively studied in the last year. Although diagnostic accuracy remains deceiving in non-Alzheimer's disease tauopathies, positron emission tomography tau tracers could be used to monitor disease progression. SUMMARY: Despite the advent of novel therapeutic approaches and the increasing number of clinical trials in tauopathies, accurate clinical diagnosis is still an unmet need and better tau biomarkers are still desperately needed. Although primary taupathies are rare and heterogeneous disorders, their combined prevalence and the importance of tau disorder in Alzheimer's disease and secondary tauopathies makes research on tauopathy a priority - because it could benefit many patients.\n
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\n  \n 2016\n \n \n (6)\n \n \n
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\n \n\n \n \n \n \n \n Multiple Simultaneous Spontaneous Intracerebral Hemorrhages: A Rare Entity.\n \n \n \n\n\n \n Chen, Y.; Hénon, H.; Bombois, S.; Pasquier, F.; and Cordonnier, C.\n\n\n \n\n\n\n Cerebrovascular Diseases (Basel, Switzerland), 41(1-2): 74–79. 2016.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{chen_multiple_2016,\n\ttitle = {Multiple {Simultaneous} {Spontaneous} {Intracerebral} {Hemorrhages}: {A} {Rare} {Entity}},\n\tvolume = {41},\n\tissn = {1421-9786},\n\tshorttitle = {Multiple {Simultaneous} {Spontaneous} {Intracerebral} {Hemorrhages}},\n\tdoi = {10.1159/000442475},\n\tabstract = {BACKGROUND: In hospital databases, multiple simultaneous spontaneous intracerebral hemorrhages (ICH-m) account for 0.7-5.6\\% of all ICHs. Their long-term outcome has never been systematically and prospectively investigated. We aimed at identifying the long-term outcome of patients with ICH-m.\nMETHODS: We prospectively recruited consecutive adults with ICH-m and followed them up for at least 4.5 years. We classified patients into the following 3 groups: (i) definite or probable cerebral amyloid angiopathy (CAA), (ii) deep perforating vasculopathy (DPV) and (iii) unknown causes.\nRESULTS: Of 562 consecutive patients with ICH, 32 had ICH-m (5.7\\%): 8 (25\\%) with probable CAA, 5 (16\\%) with DPV and 19 (59\\%) with ICH-m of undetermined cause. At the last visit (cumulative follow-up of 39.5 person-year), 27 patients (84\\%) had died, and 3 of the 5 survivors were independent. Late-onset seizures, recurrent ICH-m (symptomatic or not) and new brain microbleeds were mainly found in patients with probable CAA.\nCONCLUSIONS: ICH-m is a rare but extremely severe expression of ICH. Survivors with CAA are more likely to develop late seizures and new hemorrhagic lesions. Because of low survival rates, large multicenter cohort studies are needed for a better understanding of this rare condition.},\n\tlanguage = {eng},\n\tnumber = {1-2},\n\tjournal = {Cerebrovascular Diseases (Basel, Switzerland)},\n\tauthor = {Chen, Yaohua and Hénon, Hilde and Bombois, Stéphanie and Pasquier, Florence and Cordonnier, Charlotte},\n\tyear = {2016},\n\tpmid = {26671248},\n\tkeywords = {Aged, Aged, 80 and over, Basal Ganglia Cerebrovascular Disease, Brain, Cerebral Amyloid Angiopathy, Cerebral Hemorrhage, Cohort Studies, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Prospective Studies, Rare Diseases, Seizures},\n\tpages = {74--79},\n}\n\n
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\n BACKGROUND: In hospital databases, multiple simultaneous spontaneous intracerebral hemorrhages (ICH-m) account for 0.7-5.6% of all ICHs. Their long-term outcome has never been systematically and prospectively investigated. We aimed at identifying the long-term outcome of patients with ICH-m. METHODS: We prospectively recruited consecutive adults with ICH-m and followed them up for at least 4.5 years. We classified patients into the following 3 groups: (i) definite or probable cerebral amyloid angiopathy (CAA), (ii) deep perforating vasculopathy (DPV) and (iii) unknown causes. RESULTS: Of 562 consecutive patients with ICH, 32 had ICH-m (5.7%): 8 (25%) with probable CAA, 5 (16%) with DPV and 19 (59%) with ICH-m of undetermined cause. At the last visit (cumulative follow-up of 39.5 person-year), 27 patients (84%) had died, and 3 of the 5 survivors were independent. Late-onset seizures, recurrent ICH-m (symptomatic or not) and new brain microbleeds were mainly found in patients with probable CAA. CONCLUSIONS: ICH-m is a rare but extremely severe expression of ICH. Survivors with CAA are more likely to develop late seizures and new hemorrhagic lesions. Because of low survival rates, large multicenter cohort studies are needed for a better understanding of this rare condition.\n
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\n \n\n \n \n \n \n \n Limiting Factors of Brain Donation in Neurodegenerative Diseases: The Example of French Memory Clinics.\n \n \n \n\n\n \n Le Bouc, R.; Marelli, C.; Beaufils, E.; Berr, C.; Hommet, C.; Touchon, J.; Pasquier, F.; and Deramecourt, V.\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 49(4): 1075–1083. 2016.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{le_bouc_limiting_2016,\n\ttitle = {Limiting {Factors} of {Brain} {Donation} in {Neurodegenerative} {Diseases}: {The} {Example} of {French} {Memory} {Clinics}},\n\tvolume = {49},\n\tissn = {1875-8908},\n\tshorttitle = {Limiting {Factors} of {Brain} {Donation} in {Neurodegenerative} {Diseases}},\n\tdoi = {10.3233/JAD-150825},\n\tabstract = {Postmortem neuropathological examination of the brain is essential in neurodegenerative diseases, to ensure accurate diagnosis, to obtain an a posteriori critical assessment of the adequacy of clinical care, and to validate new biomarkers, but is only rarely performed. The purpose of this study was to assess factors limiting brain donation, such as reluctance of physicians to seek donation consent, opposition from patients and families, and organizational constraints. We conducted a survey across French memory clinics and major neuropathological centers. Few postmortem examinations were performed annually, as less than one third of the centers had performed at least five autopsies, and 41\\% had performed none. The main limiting factor was the lack of donation requests made by physicians, as half of them never approach patients for brain donation. Reasons for not seeking donation consent often include discomfort broaching the subject and lack of awareness of the medical and scientific benefit of postmortems (77\\%), organizational constraints (61\\%), and overestimation of families' negative reaction (51\\%). Family refusals represented a second major obstacle, and were often caused by misconceptions. Identifying and addressing these biases early could help improve physicians' rate of making requests and the public's awareness about the importance of brain donation.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Le Bouc, Raphael and Marelli, Cecilia and Beaufils, Emilie and Berr, Claudine and Hommet, Caroline and Touchon, Jacques and Pasquier, Florence and Deramecourt, Vincent},\n\tyear = {2016},\n\tpmid = {26756326},\n\tkeywords = {Alzheimer’s disease, Autopsy, Brain, France, Health Knowledge, Attitudes, Practice, Humans, Neurodegenerative Diseases, Physicians, Retrospective Studies, brain bank, brain donation, neurodegenerative diseases, postmortem examination},\n\tpages = {1075--1083},\n}\n\n
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\n Postmortem neuropathological examination of the brain is essential in neurodegenerative diseases, to ensure accurate diagnosis, to obtain an a posteriori critical assessment of the adequacy of clinical care, and to validate new biomarkers, but is only rarely performed. The purpose of this study was to assess factors limiting brain donation, such as reluctance of physicians to seek donation consent, opposition from patients and families, and organizational constraints. We conducted a survey across French memory clinics and major neuropathological centers. Few postmortem examinations were performed annually, as less than one third of the centers had performed at least five autopsies, and 41% had performed none. The main limiting factor was the lack of donation requests made by physicians, as half of them never approach patients for brain donation. Reasons for not seeking donation consent often include discomfort broaching the subject and lack of awareness of the medical and scientific benefit of postmortems (77%), organizational constraints (61%), and overestimation of families' negative reaction (51%). Family refusals represented a second major obstacle, and were often caused by misconceptions. Identifying and addressing these biases early could help improve physicians' rate of making requests and the public's awareness about the importance of brain donation.\n
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\n \n\n \n \n \n \n \n A Comparative Descriptive Study of Characteristics of Early- and Late-Onset Dementia Family Caregivers.\n \n \n \n\n\n \n Ducharme, F.; Lachance, L.; Kergoat, M.; Coulombe, R.; Antoine, P.; and Pasquier, F.\n\n\n \n\n\n\n American Journal of Alzheimer's Disease and Other Dementias, 31(1): 48–56. February 2016.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{ducharme_comparative_2016,\n\ttitle = {A {Comparative} {Descriptive} {Study} of {Characteristics} of {Early}- and {Late}-{Onset} {Dementia} {Family} {Caregivers}},\n\tvolume = {31},\n\tissn = {1938-2731},\n\tdoi = {10.1177/1533317515578255},\n\tabstract = {Characteristics of early- and late-onset dementia family caregivers were described and compared. Based on a theoretical model of role transition, data were collected through structured interviews from 48 caregivers of adults with Alzheimer's disease or a related dementia older than the age of 70 and 48 caregivers of similarly diagnosed adults younger than the age of 60. A significantly higher proportion of caregivers of younger adults were spouses and gainfully employed compared with those of older adults; they had more years of schooling, took care of a person with more severe impairments, received more help, perceived themselves as better prepared to deal with future needs, and better informed about services. They did not differ from caregivers of older adults in terms of psychological distress, role confidence, self-efficacy, and social support. This study highlights differences and similarities to be considered in the development of services tailored to the specific needs of each group.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {American Journal of Alzheimer's Disease and Other Dementias},\n\tauthor = {Ducharme, Francine and Lachance, Lise and Kergoat, Marie-Jeanne and Coulombe, Renée and Antoine, Pascal and Pasquier, Florence},\n\tmonth = feb,\n\tyear = {2016},\n\tpmid = {25814627},\n\tkeywords = {Adult, Aged, Aged, 80 and over, Alzheimer Disease, Canada, Caregivers, Employment, Female, Humans, Male, Middle Aged, Self Efficacy, Social Support, Spouses, Stress, Psychological, Surveys and Questionnaires, characteristics, comparative study, early-onset dementia, family caregivers, late-onset dementia},\n\tpages = {48--56},\n}\n\n
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\n Characteristics of early- and late-onset dementia family caregivers were described and compared. Based on a theoretical model of role transition, data were collected through structured interviews from 48 caregivers of adults with Alzheimer's disease or a related dementia older than the age of 70 and 48 caregivers of similarly diagnosed adults younger than the age of 60. A significantly higher proportion of caregivers of younger adults were spouses and gainfully employed compared with those of older adults; they had more years of schooling, took care of a person with more severe impairments, received more help, perceived themselves as better prepared to deal with future needs, and better informed about services. They did not differ from caregivers of older adults in terms of psychological distress, role confidence, self-efficacy, and social support. This study highlights differences and similarities to be considered in the development of services tailored to the specific needs of each group.\n
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\n \n\n \n \n \n \n \n Young onset demented patients in French cognitive-behavioral specialized units.\n \n \n \n\n\n \n Lebert, F.; Leroy, M.; Pasquier, F.; and Strubel, D.\n\n\n \n\n\n\n Geriatrie Et Psychologie Neuropsychiatrie Du Vieillissement, 14(2): 194–200. June 2016.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{lebert_young_2016,\n\ttitle = {Young onset demented patients in {French} cognitive-behavioral specialized units},\n\tvolume = {14},\n\tissn = {2115-7863},\n\tdoi = {10.1684/pnv.2016.0607},\n\tabstract = {The number of patients with young onset dementia (YOD) (first symptoms beginning before the age of 60 years) is estimated around 5,000 in France. On account of the usual severity of behavioral symptoms in these patients, the need for cognitive-behavioral specialized unit (UCC) is expected. To determine the number and characteristics of YOD patients cared for in UCC in France during the year 2013. A specific questionnaire was sent to the 84 French UCC. The questionnaire was completed by 55 UCC (65\\%), whose 33 received 179 YOD patients. The diagnosis was Alzheimer's disease in 50\\% of the cases and frontotemporal dementia in 30\\%. The main reasons for the hospitalization in UCC were the severity of behavioral symptoms in 86\\% of cases, the need to alleviate the caregiver burden in 31\\% and the waiting for a place in a nursing home in 23\\%. Mean duration of hospitalization was 40.4 ± 20.5 days. At the end of hospitalization 51\\% of the patients returned to their original living accomodation and 39\\% entered into a nursing home. The main reason of YOD patients hospitalization reject was the care team's fear in the UCC without experience. The severity of the behavioral troubles was the major issue while the necessary ethical reflection raised by the YOD patients management was a positive aspect. The teams rated how ready do they feel about taking care of YOD patients on a scale from 0 to 100, the median was 35. The welcoming of YOD patients in UCC is necessary, however the severity of the behavioral troubles and the care teams fear prompt to set up specific education and to increase of the number of staff for YOD patients management.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Geriatrie Et Psychologie Neuropsychiatrie Du Vieillissement},\n\tauthor = {Lebert, Florence and Leroy, Melanie and Pasquier, Florence and Strubel, Denise},\n\tmonth = jun,\n\tyear = {2016},\n\tpmid = {27277152},\n\tkeywords = {Age of Onset, Alzheimer Disease, Alzheimer's disease, Cognitive Behavioral Therapy, Female, France, Frontotemporal Dementia, Hospital Units, Humans, Male, Middle Aged, Psychiatric Department, Hospital, behavioral symptoms, cognitive-behavioral specialized units, frontotemporal dementia, young onset dementia},\n\tpages = {194--200},\n}\n\n
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\n The number of patients with young onset dementia (YOD) (first symptoms beginning before the age of 60 years) is estimated around 5,000 in France. On account of the usual severity of behavioral symptoms in these patients, the need for cognitive-behavioral specialized unit (UCC) is expected. To determine the number and characteristics of YOD patients cared for in UCC in France during the year 2013. A specific questionnaire was sent to the 84 French UCC. The questionnaire was completed by 55 UCC (65%), whose 33 received 179 YOD patients. The diagnosis was Alzheimer's disease in 50% of the cases and frontotemporal dementia in 30%. The main reasons for the hospitalization in UCC were the severity of behavioral symptoms in 86% of cases, the need to alleviate the caregiver burden in 31% and the waiting for a place in a nursing home in 23%. Mean duration of hospitalization was 40.4 ± 20.5 days. At the end of hospitalization 51% of the patients returned to their original living accomodation and 39% entered into a nursing home. The main reason of YOD patients hospitalization reject was the care team's fear in the UCC without experience. The severity of the behavioral troubles was the major issue while the necessary ethical reflection raised by the YOD patients management was a positive aspect. The teams rated how ready do they feel about taking care of YOD patients on a scale from 0 to 100, the median was 35. The welcoming of YOD patients in UCC is necessary, however the severity of the behavioral troubles and the care teams fear prompt to set up specific education and to increase of the number of staff for YOD patients management.\n
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\n \n\n \n \n \n \n \n Cognition and neuropsychiatry in behavioral variant frontotemporal dementia by disease stage.\n \n \n \n\n\n \n Bertoux, M.; Sarazin, M.; Pasquier, F.; Bottlaender, M.; de Souza, L. C.; Mioshi, E.; Hornberger, M.; Ranasinghe, K. G.; Rankin, K. P.; Lobach, I. V.; Kramer, J. H.; Sturm, V. E.; Bettcher, B. M.; Possin, K.; You, S. C.; Lamarre, A. K.; Shany-Ur, T.; Stephens, M. L.; Perry, D. C.; Lee, S. E.; Miller, Z. A.; Gorno-Tempini, M. L.; Rosen, H. J.; Boxer, A.; Seeley, W. W.; Rabinovici, G. D.; Vossel, K. A.; and Miller, B. L.\n\n\n \n\n\n\n Neurology, 87(14): 1523. October 2016.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{bertoux_cognition_2016,\n\ttitle = {Cognition and neuropsychiatry in behavioral variant frontotemporal dementia by disease stage},\n\tvolume = {87},\n\tissn = {1526-632X},\n\tdoi = {10.1212/01.wnl.0000503343.29930.76},\n\tlanguage = {eng},\n\tnumber = {14},\n\tjournal = {Neurology},\n\tauthor = {Bertoux, Maxime and Sarazin, Marie and Pasquier, Florence and Bottlaender, Michel and de Souza, Leonardo Cruz and Mioshi, Eneida and Hornberger, Michael and Ranasinghe, Kamalini G. and Rankin, Katherine P. and Lobach, Iryna V. and Kramer, Joel H. and Sturm, Virginia E. and Bettcher, Brianne M. and Possin, Katherine and You, S. Christine and Lamarre, Amanda K. and Shany-Ur, Tal and Stephens, Melanie L. and Perry, David C. and Lee, Suzee E. and Miller, Zachary A. and Gorno-Tempini, Maria L. and Rosen, Howard J. and Boxer, Adam and Seeley, William W. and Rabinovici, Gil D. and Vossel, Keith A. and Miller, Bruce L.},\n\tmonth = oct,\n\tyear = {2016},\n\tpmid = {27698154},\n\tpmcid = {PMC5990306},\n\tkeywords = {Cognition, Frontotemporal Dementia, Humans, Neuropsychiatry, Neuropsychological Tests},\n\tpages = {1523},\n}\n\n
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\n \n\n \n \n \n \n \n Couples' experiences with early-onset dementia: An interpretative phenomenological analysis of dyadic dynamics.\n \n \n \n\n\n \n Wawrziczny, E.; Antoine, P.; Ducharme, F.; Kergoat, M.; and Pasquier, F.\n\n\n \n\n\n\n Dementia (London, England), 15(5): 1082–1099. September 2016.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{wawrziczny_couples_2016,\n\ttitle = {Couples' experiences with early-onset dementia: {An} interpretative phenomenological analysis of dyadic dynamics},\n\tvolume = {15},\n\tissn = {1741-2684},\n\tshorttitle = {Couples' experiences with early-onset dementia},\n\tdoi = {10.1177/1471301214554720},\n\tabstract = {OBJECTIVE: The growing interest in early-onset dementia has attracted attention to the situation and experiences of the caregiver, most often the spouse. Several qualitative studies on caregiving spouses have underlined the importance of the feeling of loss, the change of role reported by the caregiving spouses, and the strategies used to protect the person with dementia, all of which raise the question of the relational dynamics at play in these dyads. The present study on 16 couples examines the experiences of each partner, as well as the kinds of interactions taking place within the dyad and how they have evolved since the disease began.\nDESIGN: An interpretative phenomenological analysis was conducted on dyadic semi-structured interviews.\nRESULTS: Seven axes emerged from the analyses, showing that control over symptoms gradually leads to deterioration of marital interactions and to the components of marital dissolution.},\n\tlanguage = {eng},\n\tnumber = {5},\n\tjournal = {Dementia (London, England)},\n\tauthor = {Wawrziczny, Emilie and Antoine, Pascal and Ducharme, Francine and Kergoat, Marie-Jeanne and Pasquier, Florence},\n\tmonth = sep,\n\tyear = {2016},\n\tpmid = {25305278},\n\tkeywords = {Adaptation, Psychological, Caregivers, Dementia, Family Characteristics, Female, Humans, Interpersonal Relations, Male, Mental Status Schedule, Middle Aged, couple, dyadic dynamic, early-onset dementia, interpretative phenomenological analysis, qualitative study},\n\tpages = {1082--1099},\n}\n\n
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\n OBJECTIVE: The growing interest in early-onset dementia has attracted attention to the situation and experiences of the caregiver, most often the spouse. Several qualitative studies on caregiving spouses have underlined the importance of the feeling of loss, the change of role reported by the caregiving spouses, and the strategies used to protect the person with dementia, all of which raise the question of the relational dynamics at play in these dyads. The present study on 16 couples examines the experiences of each partner, as well as the kinds of interactions taking place within the dyad and how they have evolved since the disease began. DESIGN: An interpretative phenomenological analysis was conducted on dyadic semi-structured interviews. RESULTS: Seven axes emerged from the analyses, showing that control over symptoms gradually leads to deterioration of marital interactions and to the components of marital dissolution.\n
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\n  \n 2015\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n Characterization and prediction of the recognition of emotional faces and emotional bursts in temporal lobe epilepsy.\n \n \n \n\n\n \n Hennion, S.; Szurhaj, W.; Duhamel, A.; Lopes, R.; Tyvaert, L.; Derambure, P.; and Delbeuck, X.\n\n\n \n\n\n\n Journal of Clinical and Experimental Neuropsychology, 37(9): 931–945. 2015.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{hennion_characterization_2015,\n\ttitle = {Characterization and prediction of the recognition of emotional faces and emotional bursts in temporal lobe epilepsy},\n\tvolume = {37},\n\tissn = {1744-411X},\n\tdoi = {10.1080/13803395.2015.1068280},\n\tabstract = {INTRODUCTION: The present study sought to characterize and predict the recognition of emotional stimuli (presented in a visual or auditory modality) by patients with temporal lobe epilepsy (TLE).\nMETHOD: Fifty TLE patients and 50 matched controls performed two emotion recognition tasks (emotional faces and emotional bursts). Neutral stimuli were also presented, and emotional biases were monitored by analyzing errors. Demographic, cognitive, psychobehavioral and (in TLE patients only) clinical and quality of life data were also recorded.\nRESULTS: Compared with controls, TLE patients were impaired in the recognition of fear expressions in both visual and auditory modality tasks. However, impairments in the two channels were not always concomitant on the individual level. In the visual modality, recognition of disgust and neutral expressions was significantly worse in TLE patients. In the auditory modality, nonsignificant trends toward poor recognition of disgust and neutral expressions were observed. Negative biases were noted in TLE patients; expressions of fear (faces and bursts) were more frequently misinterpreted as disgust, and neutral facial expressions were more frequently misinterpreted as sadness. Impairments in the recognition of facial fear were less pronounced in left TLE patients who (according to structural magnetic resonance imaging, MRI) did not have any brain lesions. In TLE patients, low levels of social support (a quality of life parameter) were associated with worse recognition of facial disgust, and higher levels of apathy were associated with better recognition of neutral faces.\nCONCLUSIONS: TLE patients are impaired in some aspects of emotion recognition with both visual and auditory stimuli, although the differential impact of TLE on these modalities requires further research. These emotional impairments are related to quality of life and psychobehavioral parameters.},\n\tlanguage = {eng},\n\tnumber = {9},\n\tjournal = {Journal of Clinical and Experimental Neuropsychology},\n\tauthor = {Hennion, Sophie and Szurhaj, William and Duhamel, Alain and Lopes, Renaud and Tyvaert, Louise and Derambure, Philippe and Delbeuck, Xavier},\n\tyear = {2015},\n\tpmid = {26332173},\n\tkeywords = {Acoustic Stimulation, Adult, Apathy, Cognition Disorders, Emotion recognition, Emotional burst, Emotional face, Emotions, Epilepsy, Temporal Lobe, Facial Expression, Female, Functional Laterality, Humans, Male, Middle Aged, Negative bias, Neuropsychological Tests, Photic Stimulation, Predictive Value of Tests, Quality of Life, Quality of life, Recognition, Psychology, Temporal lobe epilepsy},\n\tpages = {931--945},\n}\n\n
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\n INTRODUCTION: The present study sought to characterize and predict the recognition of emotional stimuli (presented in a visual or auditory modality) by patients with temporal lobe epilepsy (TLE). METHOD: Fifty TLE patients and 50 matched controls performed two emotion recognition tasks (emotional faces and emotional bursts). Neutral stimuli were also presented, and emotional biases were monitored by analyzing errors. Demographic, cognitive, psychobehavioral and (in TLE patients only) clinical and quality of life data were also recorded. RESULTS: Compared with controls, TLE patients were impaired in the recognition of fear expressions in both visual and auditory modality tasks. However, impairments in the two channels were not always concomitant on the individual level. In the visual modality, recognition of disgust and neutral expressions was significantly worse in TLE patients. In the auditory modality, nonsignificant trends toward poor recognition of disgust and neutral expressions were observed. Negative biases were noted in TLE patients; expressions of fear (faces and bursts) were more frequently misinterpreted as disgust, and neutral facial expressions were more frequently misinterpreted as sadness. Impairments in the recognition of facial fear were less pronounced in left TLE patients who (according to structural magnetic resonance imaging, MRI) did not have any brain lesions. In TLE patients, low levels of social support (a quality of life parameter) were associated with worse recognition of facial disgust, and higher levels of apathy were associated with better recognition of neutral faces. CONCLUSIONS: TLE patients are impaired in some aspects of emotion recognition with both visual and auditory stimuli, although the differential impact of TLE on these modalities requires further research. These emotional impairments are related to quality of life and psychobehavioral parameters.\n
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\n \n\n \n \n \n \n \n [Henri Petit (1932-2014)].\n \n \n \n\n\n \n Pasquier, F.\n\n\n \n\n\n\n Revue Neurologique, 171(2): 121–124. February 2015.\n \n\n\n\n
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@article{pasquier_henri_2015,\n\ttitle = {[{Henri} {Petit} (1932-2014)]},\n\tvolume = {171},\n\tissn = {0035-3787},\n\tdoi = {10.1016/j.neurol.2015.02.003},\n\tlanguage = {fre},\n\tnumber = {2},\n\tjournal = {Revue Neurologique},\n\tauthor = {Pasquier, F.},\n\tmonth = feb,\n\tyear = {2015},\n\tpmid = {26672131},\n\tkeywords = {Belgium, Biomedical Research, France, History, 20th Century, History, 21st Century, Humans, Neurology, Psychiatry, Translational Medical Research},\n\tpages = {121--124},\n}\n\n
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\n  \n 2014\n \n \n (7)\n \n \n
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\n \n\n \n \n \n \n \n Differential processing of natural scenes in posterior cortical atrophy and in Alzheimer's disease, as measured with a saccade choice task.\n \n \n \n\n\n \n Boucart, M.; Calais, G.; Lenoble, Q.; Moroni, C.; and Pasquier, F.\n\n\n \n\n\n\n Frontiers in Integrative Neuroscience, 8: 60. 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{boucart_differential_2014,\n\ttitle = {Differential processing of natural scenes in posterior cortical atrophy and in {Alzheimer}'s disease, as measured with a saccade choice task},\n\tvolume = {8},\n\tissn = {1662-5145},\n\tdoi = {10.3389/fnint.2014.00060},\n\tabstract = {Atrophy of the medial temporal lobe structures that support scene perception and the binding of an object to its context (i.e., the hippocampus and the parahippocampal cortex) appears early in the course of Alzheimer's disease (AD). However, few studies have investigated scene perception in people with AD. Here, we assessed the ability to find a target object within a natural scene in people with AD and in people with posterior cortical atrophy (PCA, a variant of AD). Pairs of color photographs were displayed on the left and right of a fixation cross for 1 s. In separate blocks of trials, participants were asked to categorize the target (an animal) by either moving their eyes toward the photograph containing the target (the saccadic choice task) or pressing a key corresponding to the target's location (the manual choice task). Isolated objects and objects within scenes were studied in both tasks. Participants with PCA were more impaired in detection of a target within a scene than participants with AD. The latter's performance pattern was more similar to that of age-matched controls in terms of accuracy, saccade latencies and the benefit gained from contextual information. Participants with PCA benefited less from contextual information in both the saccade and the manual choice tasks-suggesting that people with posterior brain lesions have impairments in figure/ground segregation and are more sensitive to object crowding.},\n\tlanguage = {eng},\n\tjournal = {Frontiers in Integrative Neuroscience},\n\tauthor = {Boucart, Muriel and Calais, Gauthier and Lenoble, Quentin and Moroni, Christine and Pasquier, Florence},\n\tyear = {2014},\n\tpmid = {25120440},\n\tpmcid = {PMC4111099},\n\tkeywords = {Alzheimer, context, posterior cortical atrophy, saccades, scene perception},\n\tpages = {60},\n}\n\n
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\n Atrophy of the medial temporal lobe structures that support scene perception and the binding of an object to its context (i.e., the hippocampus and the parahippocampal cortex) appears early in the course of Alzheimer's disease (AD). However, few studies have investigated scene perception in people with AD. Here, we assessed the ability to find a target object within a natural scene in people with AD and in people with posterior cortical atrophy (PCA, a variant of AD). Pairs of color photographs were displayed on the left and right of a fixation cross for 1 s. In separate blocks of trials, participants were asked to categorize the target (an animal) by either moving their eyes toward the photograph containing the target (the saccadic choice task) or pressing a key corresponding to the target's location (the manual choice task). Isolated objects and objects within scenes were studied in both tasks. Participants with PCA were more impaired in detection of a target within a scene than participants with AD. The latter's performance pattern was more similar to that of age-matched controls in terms of accuracy, saccade latencies and the benefit gained from contextual information. Participants with PCA benefited less from contextual information in both the saccade and the manual choice tasks-suggesting that people with posterior brain lesions have impairments in figure/ground segregation and are more sensitive to object crowding.\n
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\n \n\n \n \n \n \n \n Neuronal substrate of cognitive impairment in post-stroke dementia.\n \n \n \n\n\n \n Deramecourt, V.; and Pasquier, F.\n\n\n \n\n\n\n Brain: A Journal of Neurology, 137(Pt 9): 2404–2405. September 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{deramecourt_neuronal_2014,\n\ttitle = {Neuronal substrate of cognitive impairment in post-stroke dementia},\n\tvolume = {137},\n\tissn = {1460-2156},\n\tdoi = {10.1093/brain/awu188},\n\tlanguage = {eng},\n\tnumber = {Pt 9},\n\tjournal = {Brain: A Journal of Neurology},\n\tauthor = {Deramecourt, Vincent and Pasquier, Florence},\n\tmonth = sep,\n\tyear = {2014},\n\tpmid = {25125586},\n\tkeywords = {Aging, Dementia, Vascular, Female, Humans, Male, Prefrontal Cortex, Pyramidal Cells},\n\tpages = {2404--2405},\n}\n\n
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\n \n\n \n \n \n \n \n Treatment of sleep apnoea syndrome decreases cognitive decline in patients with Alzheimer's disease.\n \n \n \n\n\n \n Troussière, A.; Charley, C. M.; Salleron, J.; Richard, F.; Delbeuck, X.; Derambure, P.; Pasquier, F.; and Bombois, S.\n\n\n \n\n\n\n Journal of Neurology, Neurosurgery, and Psychiatry, 85(12): 1405–1408. December 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{troussiere_treatment_2014,\n\ttitle = {Treatment of sleep apnoea syndrome decreases cognitive decline in patients with {Alzheimer}'s disease},\n\tvolume = {85},\n\tissn = {1468-330X},\n\tdoi = {10.1136/jnnp-2013-307544},\n\tabstract = {BACKGROUND: It is essential to detect and then treat factors that aggravate Alzheimer's disease (AD). Here, we sought to determine whether or not continuous positive airway pressure (CPAP) therapy for sleep apnoea syndrome (SAS) slows the rate of cognitive decline in mild-to-moderate AD patients.\nMETHODS: Between January 2003 and June 2011, we included consecutive, mild-to-moderate AD patients (a Mini Mental State Examination (MMSE) score at inclusion ≥15) with severe SAS as determined by video-polysomnography (an apnoea-hypopnoea index ≥30). In this single-blind, proof-of-concept trial, we analysed the mean decline in the annual MMSE score (the main outcome measure) according to whether or not the patients had received CPAP therapy. The decline was computed for each patient and for the first 3 years of follow-up.\nRESULTS: Of the 23 included patients, 14 underwent CPAP treatment. The CPAP and non-CPAP groups did not differ significantly in terms of their demographic characteristics or MMSE score at baseline. The median annual MMSE decline was significantly slower in the CPAP group (-0.7 (-1.7; +0.8)) than in the non-CPAP group (-2.2 (-3.3; -1.9); p=0.013).\nCONCLUSIONS: In this pilot study, CPAP treatment of severe SAS in mild-to-moderate AD patients was associated with significantly slower cognitive decline over a three-year follow-up period. Our results emphasise the importance of detecting and treating SAS in this population.},\n\tlanguage = {eng},\n\tnumber = {12},\n\tjournal = {Journal of Neurology, Neurosurgery, and Psychiatry},\n\tauthor = {Troussière, Anne-Cécile and Charley, Christelle Monaca and Salleron, Julia and Richard, Florence and Delbeuck, Xavier and Derambure, Philippe and Pasquier, Florence and Bombois, Stéphanie},\n\tmonth = dec,\n\tyear = {2014},\n\tpmid = {24828897},\n\tkeywords = {Aged, Alzheimer Disease, Alzheimer's Disease, CSF, Cognition, Continuous Positive Airway Pressure, Disease Progression, Female, Humans, Male, Neuropsychological Tests, Polysomnography, Single-Blind Method, Sleep Apnea Syndromes, Sleep Apnoea},\n\tpages = {1405--1408},\n}\n\n
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\n BACKGROUND: It is essential to detect and then treat factors that aggravate Alzheimer's disease (AD). Here, we sought to determine whether or not continuous positive airway pressure (CPAP) therapy for sleep apnoea syndrome (SAS) slows the rate of cognitive decline in mild-to-moderate AD patients. METHODS: Between January 2003 and June 2011, we included consecutive, mild-to-moderate AD patients (a Mini Mental State Examination (MMSE) score at inclusion ≥15) with severe SAS as determined by video-polysomnography (an apnoea-hypopnoea index ≥30). In this single-blind, proof-of-concept trial, we analysed the mean decline in the annual MMSE score (the main outcome measure) according to whether or not the patients had received CPAP therapy. The decline was computed for each patient and for the first 3 years of follow-up. RESULTS: Of the 23 included patients, 14 underwent CPAP treatment. The CPAP and non-CPAP groups did not differ significantly in terms of their demographic characteristics or MMSE score at baseline. The median annual MMSE decline was significantly slower in the CPAP group (-0.7 (-1.7; +0.8)) than in the non-CPAP group (-2.2 (-3.3; -1.9); p=0.013). CONCLUSIONS: In this pilot study, CPAP treatment of severe SAS in mild-to-moderate AD patients was associated with significantly slower cognitive decline over a three-year follow-up period. Our results emphasise the importance of detecting and treating SAS in this population.\n
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\n \n\n \n \n \n \n \n Animal spotting in Alzheimer's disease: an eye tracking study of object categorization.\n \n \n \n\n\n \n Boucart, M.; Bubbico, G.; Szaffarczyk, S.; and Pasquier, F.\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 39(1): 181–189. 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{boucart_animal_2014,\n\ttitle = {Animal spotting in {Alzheimer}'s disease: an eye tracking study of object categorization},\n\tvolume = {39},\n\tissn = {1875-8908},\n\tshorttitle = {Animal spotting in {Alzheimer}'s disease},\n\tdoi = {10.3233/JAD-131331},\n\tabstract = {We investigated rapid object categorization and, more specifically, the ability to detect a target object within a natural scene in people with mild Alzheimer's disease (AD) using a saccadic choice task. It has been suggested that the anatomical pathway likely used to initiate rapid oculomotor responses in the saccadic choice task could involve the Frontal Eye Field, a structure that is part of the dorsal attentional network, in which connectivity is disrupted in AD. Seventeen patients with mild AD and 23 healthy age-matched controls took part in the study. A group of 24 young healthy observers was included as it has been reported that normal aging affects eye movements. Participants were presented with pairs of colored photographs of natural scenes, one containing an animal (the target) and one containing various objects (distracter), displayed for 1 s left and right of fixation. They were asked to saccade to the scene containing an animal. Neither pathology nor age affected temporal (saccade latencies and durations) and spatial (saccade amplitude) parameters of eye movements. Patients with AD were significantly less accurate than age-matched controls, and older participants were less accurate than young observers. The results are interpreted in terms of noisier sensory information and increased uncertainty in relation to deficits in the magnocellular pathway. The results suggest that, even at a mild stage of the pathology, people exhibit difficulties in selecting relevant objects.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Boucart, Muriel and Bubbico, Giovanna and Szaffarczyk, Sébastien and Pasquier, Florence},\n\tyear = {2014},\n\tpmid = {24121969},\n\tkeywords = {Adult, Aged, Aging, Alzheimer Disease, Alzheimer's disease, Analysis of Variance, Animals, Attention, Calibration, Female, Humans, Male, Reaction Time, Saccades, Visual Perception, eye movements, saccade, scene perception},\n\tpages = {181--189},\n}\n\n
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\n We investigated rapid object categorization and, more specifically, the ability to detect a target object within a natural scene in people with mild Alzheimer's disease (AD) using a saccadic choice task. It has been suggested that the anatomical pathway likely used to initiate rapid oculomotor responses in the saccadic choice task could involve the Frontal Eye Field, a structure that is part of the dorsal attentional network, in which connectivity is disrupted in AD. Seventeen patients with mild AD and 23 healthy age-matched controls took part in the study. A group of 24 young healthy observers was included as it has been reported that normal aging affects eye movements. Participants were presented with pairs of colored photographs of natural scenes, one containing an animal (the target) and one containing various objects (distracter), displayed for 1 s left and right of fixation. They were asked to saccade to the scene containing an animal. Neither pathology nor age affected temporal (saccade latencies and durations) and spatial (saccade amplitude) parameters of eye movements. Patients with AD were significantly less accurate than age-matched controls, and older participants were less accurate than young observers. The results are interpreted in terms of noisier sensory information and increased uncertainty in relation to deficits in the magnocellular pathway. The results suggest that, even at a mild stage of the pathology, people exhibit difficulties in selecting relevant objects.\n
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\n \n\n \n \n \n \n \n Unmet support needs of early-onset dementia family caregivers: a mixed-design study.\n \n \n \n\n\n \n Ducharme, F.; Kergoat, M.; Coulombe, R.; Lévesque, L.; Antoine, P.; and Pasquier, F.\n\n\n \n\n\n\n BMC nursing, 13(1): 49. 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{ducharme_unmet_2014,\n\ttitle = {Unmet support needs of early-onset dementia family caregivers: a mixed-design study},\n\tvolume = {13},\n\tissn = {1472-6955},\n\tshorttitle = {Unmet support needs of early-onset dementia family caregivers},\n\tdoi = {10.1186/s12912-014-0049-3},\n\tabstract = {BACKGROUND: Though advances in knowledge and diagnostics make it possible today to identify persons with early-onset dementia or a related cognitive disorder much sooner, little is known about the support needs of the family caregivers of these persons. The aim of this study was to document the unmet support needs of this specific group of caregivers. This knowledge is essential to open avenues for the development of innovative interventions and professional services tailored to their specific needs.\nMETHODS: This study was conducted using a mixed research design. Participants were 32 family caregivers in their 50s recruited through memory clinics and Alzheimer Societies in Quebec (Canada). The Family Caregivers Support Agreement (FCSA) tool, based on a partnership approach between caregiver and assessor, was used to collect data in the course of a semi-structured interview, combined with open-ended questions.\nRESULTS: The unmet support needs reported by nearly 70\\% of the caregivers were primarily of a psycho-educational nature. Caregivers wished primarily: (1) to receive more information on available help and financial resources; (2) to have their relatives feel valued as persons and to offer them stimulating activities adjusted to their residual abilities; (3) to reduce stress stemming from their caregiver role assumed at an early age and to have the chance to enjoy more time for themselves; and (4) to receive help at the right time and for the help to be tailored to their situation of caregiver of a young person.\nCONCLUSIONS: Results show numerous unmet support needs, including some specific to this group of family caregivers. Use of the FCSA tool allowed accurately assessing the needs that emerged from mutual exchanges. Avenues for professional innovative interventions are proposed.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {BMC nursing},\n\tauthor = {Ducharme, Francine and Kergoat, Marie-Jeanne and Coulombe, Renée and Lévesque, Louise and Antoine, Pascal and Pasquier, Florence},\n\tyear = {2014},\n\tpmid = {25550685},\n\tpmcid = {PMC4279790},\n\tkeywords = {Caregivers, Early-onset dementia, Partnership approach, Professional interventions, Unmet support needs},\n\tpages = {49},\n}\n\n
\n
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\n BACKGROUND: Though advances in knowledge and diagnostics make it possible today to identify persons with early-onset dementia or a related cognitive disorder much sooner, little is known about the support needs of the family caregivers of these persons. The aim of this study was to document the unmet support needs of this specific group of caregivers. This knowledge is essential to open avenues for the development of innovative interventions and professional services tailored to their specific needs. METHODS: This study was conducted using a mixed research design. Participants were 32 family caregivers in their 50s recruited through memory clinics and Alzheimer Societies in Quebec (Canada). The Family Caregivers Support Agreement (FCSA) tool, based on a partnership approach between caregiver and assessor, was used to collect data in the course of a semi-structured interview, combined with open-ended questions. RESULTS: The unmet support needs reported by nearly 70% of the caregivers were primarily of a psycho-educational nature. Caregivers wished primarily: (1) to receive more information on available help and financial resources; (2) to have their relatives feel valued as persons and to offer them stimulating activities adjusted to their residual abilities; (3) to reduce stress stemming from their caregiver role assumed at an early age and to have the chance to enjoy more time for themselves; and (4) to receive help at the right time and for the help to be tailored to their situation of caregiver of a young person. CONCLUSIONS: Results show numerous unmet support needs, including some specific to this group of family caregivers. Use of the FCSA tool allowed accurately assessing the needs that emerged from mutual exchanges. Avenues for professional innovative interventions are proposed.\n
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\n \n\n \n \n \n \n \n Unusual features of Creutzfeldt-Jakob disease followed-up in a memory clinic.\n \n \n \n\n\n \n Jacquin, A.; Deramecourt, V.; Bakchine, S.; Maurage, C.; and Pasquier, F.\n\n\n \n\n\n\n Journal of Neurology, 261(4): 696–701. April 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{jacquin_unusual_2014,\n\ttitle = {Unusual features of {Creutzfeldt}-{Jakob} disease followed-up in a memory clinic},\n\tvolume = {261},\n\tissn = {1432-1459},\n\tdoi = {10.1007/s00415-014-7246-6},\n\tabstract = {Sporadic Creutzfeldt-Jakob disease (sCJD) generally manifests itself by cognitive or rapidly progressive motor symptoms. An atypical onset or an unusual evolution may delay the diagnosis. Among patients with a confirmed diagnosis of sCJD following a post-mortem neuropathological examination at the Neuropathology Centre of Lille, France, those who had presented with atypical cognitive disorders at onset were included in the study. Four patients were included. The first patient (64-years-old) presented early language disorders, later accompanied by apathy and behavioral disorders. The prolonged course suggested a diagnosis of progressive primary aphasia. The second patient (68-years-old) presented with aphasia, apraxia, and ataxia of the right upper limb with parkinsonian syndrome, suggesting corticobasal degeneration. In the two last patients (58- and 61-years-old), the onset was marked by an anxiety-depression syndrome, falls, visual hallucinations, extra-pyramidal syndrome, and fluctuating cognitive decline. The diagnosis raised was probable Lewy body dementia. The 14.3.3 protein was found in two of the four cases. The clinical elements found may initially suggest focal atrophy or Lewy body dementia. A very rapid clinical deterioration generally suggests sCJD, but in the last case, the evolution was particularly slow. The diagnosis of sCJD must be considered in cases of rapid-onset dementia, even if all of the clinical criteria are not present. The detection of the 14.3.3 protein and multifold increase in total-Tau with normal or slightly increased phosphorylated-Tau in the CSF are additional arguments to reinforce the diagnosis. The post-mortem neuropathological examination is important to confirm the diagnosis.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of Neurology},\n\tauthor = {Jacquin, Agnès and Deramecourt, Vincent and Bakchine, Serge and Maurage, Claude-Alain and Pasquier, Florence},\n\tmonth = apr,\n\tyear = {2014},\n\tpmid = {24477491},\n\tkeywords = {14-3-3 Proteins, Autopsy, Creutzfeldt-Jakob Syndrome, Delayed Diagnosis, Female, Humans, Language Disorders, Male, Memory Disorders, Mental Disorders, Middle Aged, Neuropsychological Tests, Prions, Psychiatric Status Rating Scales},\n\tpages = {696--701},\n}\n\n
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\n Sporadic Creutzfeldt-Jakob disease (sCJD) generally manifests itself by cognitive or rapidly progressive motor symptoms. An atypical onset or an unusual evolution may delay the diagnosis. Among patients with a confirmed diagnosis of sCJD following a post-mortem neuropathological examination at the Neuropathology Centre of Lille, France, those who had presented with atypical cognitive disorders at onset were included in the study. Four patients were included. The first patient (64-years-old) presented early language disorders, later accompanied by apathy and behavioral disorders. The prolonged course suggested a diagnosis of progressive primary aphasia. The second patient (68-years-old) presented with aphasia, apraxia, and ataxia of the right upper limb with parkinsonian syndrome, suggesting corticobasal degeneration. In the two last patients (58- and 61-years-old), the onset was marked by an anxiety-depression syndrome, falls, visual hallucinations, extra-pyramidal syndrome, and fluctuating cognitive decline. The diagnosis raised was probable Lewy body dementia. The 14.3.3 protein was found in two of the four cases. The clinical elements found may initially suggest focal atrophy or Lewy body dementia. A very rapid clinical deterioration generally suggests sCJD, but in the last case, the evolution was particularly slow. The diagnosis of sCJD must be considered in cases of rapid-onset dementia, even if all of the clinical criteria are not present. The detection of the 14.3.3 protein and multifold increase in total-Tau with normal or slightly increased phosphorylated-Tau in the CSF are additional arguments to reinforce the diagnosis. The post-mortem neuropathological examination is important to confirm the diagnosis.\n
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\n \n\n \n \n \n \n \n Cerebral amyloid angiopathy revealed by rapidly progressing leptomeningeal lesions.\n \n \n \n\n\n \n Chouraki, A.; Rollin-Sillaire, A.; Deramecourt, V.; Zairi, F.; Le Rhun, E.; Cordonnier, C.; Delmaire, C.; Maurage, C.; and Pasquier, F.\n\n\n \n\n\n\n Journal of Neurology, 261(7): 1432–1435. July 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{chouraki_cerebral_2014,\n\ttitle = {Cerebral amyloid angiopathy revealed by rapidly progressing leptomeningeal lesions},\n\tvolume = {261},\n\tissn = {1432-1459},\n\tdoi = {10.1007/s00415-014-7378-8},\n\tlanguage = {eng},\n\tnumber = {7},\n\tjournal = {Journal of Neurology},\n\tauthor = {Chouraki, Armelle and Rollin-Sillaire, Adeline and Deramecourt, Vincent and Zairi, Fahed and Le Rhun, Emilie and Cordonnier, Charlotte and Delmaire, Christine and Maurage, Claude-Alain and Pasquier, Florence},\n\tmonth = jul,\n\tyear = {2014},\n\tpmid = {24859330},\n\tkeywords = {Antigens, CD, Antigens, Differentiation, Myelomonocytic, Brain, CD3 Complex, Cerebral Amyloid Angiopathy, Disease Progression, Electroencephalography, Female, Humans, Magnetic Resonance Imaging, Meninges, Middle Aged},\n\tpages = {1432--1435},\n}\n\n
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\n \n\n \n \n \n \n \n Neuropathology of frontotemporal lobar degeneration: a review.\n \n \n \n\n\n \n Bahia, V. S.; Takada, L. T.; and Deramecourt, V.\n\n\n \n\n\n\n Dementia & Neuropsychologia, 7(1): 19–26. March 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{bahia_neuropathology_2013,\n\ttitle = {Neuropathology of frontotemporal lobar degeneration: a review},\n\tvolume = {7},\n\tissn = {1980-5764},\n\tshorttitle = {Neuropathology of frontotemporal lobar degeneration},\n\tdoi = {10.1590/S1980-57642013DN70100004},\n\tabstract = {Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. Three main clinical variants are widely recognized within the FTLD spectrum: the behavioural variant of frontotemporal dementia (bvFTD), semantic dementia (SD) and progressive non-fluent aphasia (PNFA). FTLD represents a highly heterogeneous group of neurodegenerative disorders which are best classified according to the main protein component of pathological neuronal and glial inclusions. The most common pathological class of FTLD is associated with the TDP-43 protein (FTLD-TDP), while FTLD-Tau is considered slightly less common while the FTLD-FUS (Fused in sarcoma protein) pathology is rare. In this review, these three major pathological types of FTLD are discussed.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Dementia \\& Neuropsychologia},\n\tauthor = {Bahia, Valéria Santoro and Takada, Leonel Tadao and Deramecourt, Vincent},\n\tmonth = mar,\n\tyear = {2013},\n\tpmid = {29213815},\n\tpmcid = {PMC5619540},\n\tkeywords = {FUS, TAU, TDP, frontotemporal lobar degeneration, pathology},\n\tpages = {19--26},\n}\n\n
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\n Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. Three main clinical variants are widely recognized within the FTLD spectrum: the behavioural variant of frontotemporal dementia (bvFTD), semantic dementia (SD) and progressive non-fluent aphasia (PNFA). FTLD represents a highly heterogeneous group of neurodegenerative disorders which are best classified according to the main protein component of pathological neuronal and glial inclusions. The most common pathological class of FTLD is associated with the TDP-43 protein (FTLD-TDP), while FTLD-Tau is considered slightly less common while the FTLD-FUS (Fused in sarcoma protein) pathology is rare. In this review, these three major pathological types of FTLD are discussed.\n
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\n \n\n \n \n \n \n \n Reasons that prevent the inclusion of Alzheimer's disease patients in clinical trials.\n \n \n \n\n\n \n Rollin-Sillaire, A.; Breuilh, L.; Salleron, J.; Bombois, S.; Cassagnaud, P.; Deramecourt, V.; Mackowiak, M.; and Pasquier, F.\n\n\n \n\n\n\n British Journal of Clinical Pharmacology, 75(4): 1089–1097. April 2013.\n \n\n\n\n
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@article{rollin-sillaire_reasons_2013,\n\ttitle = {Reasons that prevent the inclusion of {Alzheimer}'s disease patients in clinical trials},\n\tvolume = {75},\n\tissn = {1365-2125},\n\tdoi = {10.1111/j.1365-2125.2012.04423.x},\n\tabstract = {AIM: To assess reasons that prevent Alzheimer's disease (AD) patients from being included in clinical trials.\nMETHODS: In 2009, we reviewed the Lille Memory Clinic's case database to identify patients suitable for inclusion in four AD clinical trials. An initial selection was made on the basis of four criteria: (i) a diagnosis of AD (with or without white matter lesions [WML]), (ii) age, (iii) mini mental state examination (MMSE) score and (iv) symptomatic treatment of AD (cholinesterase inhibitors/memantine). Next, data on patients fulfilling these criteria were reviewed against all the inclusion/exclusion criteria for four clinical trials performed in 2009 at the Memory Clinic. Reasons for non-inclusion were analyzed.\nRESULTS: Two hundred and five patients were selected according to the four initial criteria. Reasons for subsequently not including some of patients in clinical trials were abnormalities on MRI (56.9\\%, 88.9\\% of which were WML), unauthorized medication (37.3\\%), the lack of a study partner/informant (37.1\\%), the presence of a non-authorized disease (24.4\\%), contraindication to MRI (9\\%), a change in diagnosis over time (3.9\\%), visual/auditory impairments (2.9\\%), alcohol abuse (2\\%) and an insufficient educational level (1\\%).\nCONCLUSION: A high proportion of AD patients presented with vascular abnormalities on MRI. This was not unexpected, since the patients were selected from the database and, as shown in epidemiologic studies, cerebrovascular diseases are frequently associated with AD. The presence of a study partner is essential for enabling a patient to participate in clinical trials because of the need to record reliably primary and secondary outcomes.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {British Journal of Clinical Pharmacology},\n\tauthor = {Rollin-Sillaire, Adeline and Breuilh, Laetitia and Salleron, Julia and Bombois, Stéphanie and Cassagnaud, Pascaline and Deramecourt, Vincent and Mackowiak, Marie-Anne and Pasquier, Florence},\n\tmonth = apr,\n\tyear = {2013},\n\tpmid = {22891847},\n\tpmcid = {PMC3612727},\n\tkeywords = {Aged, Aged, 80 and over, Alzheimer Disease, Double-Blind Method, Humans, Middle Aged, Patient Selection, Randomized Controlled Trials as Topic},\n\tpages = {1089--1097},\n}\n\n
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\n AIM: To assess reasons that prevent Alzheimer's disease (AD) patients from being included in clinical trials. METHODS: In 2009, we reviewed the Lille Memory Clinic's case database to identify patients suitable for inclusion in four AD clinical trials. An initial selection was made on the basis of four criteria: (i) a diagnosis of AD (with or without white matter lesions [WML]), (ii) age, (iii) mini mental state examination (MMSE) score and (iv) symptomatic treatment of AD (cholinesterase inhibitors/memantine). Next, data on patients fulfilling these criteria were reviewed against all the inclusion/exclusion criteria for four clinical trials performed in 2009 at the Memory Clinic. Reasons for non-inclusion were analyzed. RESULTS: Two hundred and five patients were selected according to the four initial criteria. Reasons for subsequently not including some of patients in clinical trials were abnormalities on MRI (56.9%, 88.9% of which were WML), unauthorized medication (37.3%), the lack of a study partner/informant (37.1%), the presence of a non-authorized disease (24.4%), contraindication to MRI (9%), a change in diagnosis over time (3.9%), visual/auditory impairments (2.9%), alcohol abuse (2%) and an insufficient educational level (1%). CONCLUSION: A high proportion of AD patients presented with vascular abnormalities on MRI. This was not unexpected, since the patients were selected from the database and, as shown in epidemiologic studies, cerebrovascular diseases are frequently associated with AD. The presence of a study partner is essential for enabling a patient to participate in clinical trials because of the need to record reliably primary and secondary outcomes.\n
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\n \n\n \n \n \n \n \n Emotional and psychological implications of early AD diagnosis.\n \n \n \n\n\n \n Antoine, P.; and Pasquier, F.\n\n\n \n\n\n\n The Medical Clinics of North America, 97(3): 459–475. May 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{antoine_emotional_2013,\n\ttitle = {Emotional and psychological implications of early {AD} diagnosis},\n\tvolume = {97},\n\tissn = {1557-9859},\n\tdoi = {10.1016/j.mcna.2012.12.015},\n\tabstract = {This article reviews the current recommendations in early diagnosis and the desires of the patients and their relatives, put in perspective with the reality of the clinical practices. More specific situations covered are: (1) the issue of young diseased patients, taking into account the psychological implications of the early occurrence of the disease in life and of the longer delay for these patients between the first observable signs and the diagnosis and (2) the issue of genetic testing, taking into account the implications of this extremely early form of bad news on the individual's existence and on the family structure.},\n\tlanguage = {eng},\n\tnumber = {3},\n\tjournal = {The Medical Clinics of North America},\n\tauthor = {Antoine, Pascal and Pasquier, Florence},\n\tmonth = may,\n\tyear = {2013},\n\tpmid = {23642581},\n\tkeywords = {Aged, Alzheimer Disease, Asymptomatic Diseases, Caregivers, Cognitive Dysfunction, Communication, Cooperative Behavior, Cost of Illness, Early Diagnosis, Emotions, Genetic Testing, Humans, Interdisciplinary Communication, Patient Care Team, Practice Guidelines as Topic, Prognosis, Social Environment, Truth Disclosure},\n\tpages = {459--475},\n}\n\n
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\n This article reviews the current recommendations in early diagnosis and the desires of the patients and their relatives, put in perspective with the reality of the clinical practices. More specific situations covered are: (1) the issue of young diseased patients, taking into account the psychological implications of the early occurrence of the disease in life and of the longer delay for these patients between the first observable signs and the diagnosis and (2) the issue of genetic testing, taking into account the implications of this extremely early form of bad news on the individual's existence and on the family structure.\n
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\n \n\n \n \n \n \n \n Microbleeds in postmortem brains of patients with Alzheimer disease: a T2*-weighted gradient-echo 7.0 T magnetic resonance imaging study.\n \n \n \n\n\n \n De Reuck, J. L.; Cordonnier, C.; Deramecourt, V.; Auger, F.; Durieux, N.; Bordet, R.; Maurage, C.; Leys, D.; and Pasquier, F.\n\n\n \n\n\n\n Alzheimer Disease and Associated Disorders, 27(2): 162–167. June 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{de_reuck_microbleeds_2013,\n\ttitle = {Microbleeds in postmortem brains of patients with {Alzheimer} disease: a {T2}*-weighted gradient-echo 7.0 {T} magnetic resonance imaging study},\n\tvolume = {27},\n\tissn = {1546-4156},\n\tshorttitle = {Microbleeds in postmortem brains of patients with {Alzheimer} disease},\n\tdoi = {10.1097/WAD.0b013e318256ecd8},\n\tabstract = {This study aims to determine the distribution and to quantify microbleeds (MBs) in postmortem brains of patients with Alzheimer disease (AD) on T2*-weighted gradient-echo 7.0 T magnetic resonance imaging. Twenty-eight AD brains were compared with 5 controls. The AD brains were subdivided further: 18 without and 10 with additional severe cerebral amyloid angiopathy (AD-CAA). The distribution and the number of cortical focal signal intensity losses, representing MBs, were assessed on coronal sections at the frontal, the central, and the occipital level of a cerebral hemisphere. MBs prevailed in the central sections (P=0.005) of AD brains without CAA, whereas in AD-CAA brains, they were more frequent in all coronal sections (P≤0.002). They prevailed in the deep cortical layers of the AD brains and of the controls (P≤0.03). They were significantly increased in all cortical layers of the AD-CAA brains (P≤0.04), compared with the controls. MBs prevalence in brains of AD patients had a different topographic distribution according to the absence or presence of severe CAA.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Alzheimer Disease and Associated Disorders},\n\tauthor = {De Reuck, Jacques L. and Cordonnier, Charlotte and Deramecourt, Vincent and Auger, Florent and Durieux, Nicolas and Bordet, Regis and Maurage, Claude-Alain and Leys, Didier and Pasquier, Florence},\n\tmonth = jun,\n\tyear = {2013},\n\tpmid = {22546781},\n\tkeywords = {Aged, Aged, 80 and over, Alzheimer Disease, Autopsy, Cerebral Amyloid Angiopathy, Cerebral Hemorrhage, Female, Humans, Magnetic Resonance Imaging, Male},\n\tpages = {162--167},\n}\n\n
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\n This study aims to determine the distribution and to quantify microbleeds (MBs) in postmortem brains of patients with Alzheimer disease (AD) on T2*-weighted gradient-echo 7.0 T magnetic resonance imaging. Twenty-eight AD brains were compared with 5 controls. The AD brains were subdivided further: 18 without and 10 with additional severe cerebral amyloid angiopathy (AD-CAA). The distribution and the number of cortical focal signal intensity losses, representing MBs, were assessed on coronal sections at the frontal, the central, and the occipital level of a cerebral hemisphere. MBs prevailed in the central sections (P=0.005) of AD brains without CAA, whereas in AD-CAA brains, they were more frequent in all coronal sections (P≤0.002). They prevailed in the deep cortical layers of the AD brains and of the controls (P≤0.03). They were significantly increased in all cortical layers of the AD-CAA brains (P≤0.04), compared with the controls. MBs prevalence in brains of AD patients had a different topographic distribution according to the absence or presence of severe CAA.\n
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\n \n\n \n \n \n \n \n Memory loss during lenalidomide treatment: a report on two cases.\n \n \n \n\n\n \n Rollin-Sillaire, A.; Delbeuck, X.; Pollet, M.; Mackowiak, M.; Lenfant, P.; Noel, M.; Facon, T.; Leleu, X.; Pasquier, F.; and Le Rhun, E.\n\n\n \n\n\n\n BMC pharmacology & toxicology, 14: 41. August 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{rollin-sillaire_memory_2013,\n\ttitle = {Memory loss during lenalidomide treatment: a report on two cases},\n\tvolume = {14},\n\tissn = {2050-6511},\n\tshorttitle = {Memory loss during lenalidomide treatment},\n\tdoi = {10.1186/2050-6511-14-41},\n\tabstract = {BACKGROUND: There are many reports of cognitive dysfunction in patients receiving chemotherapy or targeted therapies. Many antineoplastic agents may be involved in the condition also known as "chemo brain" or "chemo fog".\nCASE PRESENTATION: Two male patients (aged 41 and 70) with multiple myeloma developed severe, rapidly progressing cognitive impairment (mostly involving episodic memory) and loss of independence in activities of daily living during lenalidomide-based treatment. On withdrawal of the drug, one patient recovered normal cognitive function and independence in activities of daily living, whereas mild cognitive impairment persisted in the other patient. The Naranjo Adverse Drug Reaction Probability Scale score was 6 out of 13 for the first patient and 5 out of 13 for the second, suggesting a probable causal relationship between the adverse event and lenalidomide administration.\nCONCLUSION: Lenalidomide may induce particular cognitive disorders (notably episodic memory impairments) in some patients. The drug's putative neurotoxicity is probably promoted by specific risk factors (such as previous chemotherapy, prior mild cognitive impairment, age and the presence of cerebrovascular lesions).},\n\tlanguage = {eng},\n\tjournal = {BMC pharmacology \\& toxicology},\n\tauthor = {Rollin-Sillaire, Adeline and Delbeuck, Xavier and Pollet, Marianne and Mackowiak, Marie-Anne and Lenfant, Pierre and Noel, Marie-Pierre and Facon, Thierry and Leleu, Xavier and Pasquier, Florence and Le Rhun, Emilie},\n\tmonth = aug,\n\tyear = {2013},\n\tpmid = {23937917},\n\tpmcid = {PMC3751879},\n\tkeywords = {Adult, Aged, Angiogenesis Inhibitors, Humans, Immunologic Factors, Lenalidomide, Male, Memory Disorders, Multiple Myeloma, Thalidomide, Tomography, Emission-Computed, Single-Photon},\n\tpages = {41},\n}\n\n
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\n BACKGROUND: There are many reports of cognitive dysfunction in patients receiving chemotherapy or targeted therapies. Many antineoplastic agents may be involved in the condition also known as \"chemo brain\" or \"chemo fog\". CASE PRESENTATION: Two male patients (aged 41 and 70) with multiple myeloma developed severe, rapidly progressing cognitive impairment (mostly involving episodic memory) and loss of independence in activities of daily living during lenalidomide-based treatment. On withdrawal of the drug, one patient recovered normal cognitive function and independence in activities of daily living, whereas mild cognitive impairment persisted in the other patient. The Naranjo Adverse Drug Reaction Probability Scale score was 6 out of 13 for the first patient and 5 out of 13 for the second, suggesting a probable causal relationship between the adverse event and lenalidomide administration. CONCLUSION: Lenalidomide may induce particular cognitive disorders (notably episodic memory impairments) in some patients. The drug's putative neurotoxicity is probably promoted by specific risk factors (such as previous chemotherapy, prior mild cognitive impairment, age and the presence of cerebrovascular lesions).\n
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\n \n\n \n \n \n \n \n [Dementia: new concepts, new goals].\n \n \n \n\n\n \n Pour le comité d’organisation; Hannequin, D.; Amieva, H.; Dubois, B.; Godefroy, O.; and Pasquier, F.\n\n\n \n\n\n\n Revue Neurologique, 169(10): 677–679. October 2013.\n \n\n\n\n
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@article{pour_le_comite_dorganisation_dementia_2013,\n\ttitle = {[{Dementia}: new concepts, new goals]},\n\tvolume = {169},\n\tissn = {0035-3787},\n\tshorttitle = {[{Dementia}},\n\tdoi = {10.1016/j.neurol.2013.09.002},\n\tlanguage = {fre},\n\tnumber = {10},\n\tjournal = {Revue Neurologique},\n\tauthor = {{Pour le comité d’organisation} and Hannequin, D. and Amieva, H. and Dubois, B. and Godefroy, O. and Pasquier, F.},\n\tmonth = oct,\n\tyear = {2013},\n\tpmid = {24074818},\n\tkeywords = {Alzheimer Disease, Concept Formation, Congresses as Topic, Dementia, Dementia, Vascular, Frontotemporal Lobar Degeneration, Goals, Humans},\n\tpages = {677--679},\n}\n\n
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\n \n\n \n \n \n \n \n Action and noun fluency testing to distinguish between Alzheimer's disease and dementia with Lewy bodies.\n \n \n \n\n\n \n Delbeuck, X.; Debachy, B.; Pasquier, F.; and Moroni, C.\n\n\n \n\n\n\n Journal of Clinical and Experimental Neuropsychology, 35(3): 259–268. 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{delbeuck_action_2013,\n\ttitle = {Action and noun fluency testing to distinguish between {Alzheimer}'s disease and dementia with {Lewy} bodies},\n\tvolume = {35},\n\tissn = {1744-411X},\n\tdoi = {10.1080/13803395.2013.763907},\n\tabstract = {The objective of the present study was to establish whether performance in an action fluency task is of value in the differential diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). After collecting normative data on performance in an action fluency task and a conventional animal fluency task in a cohort of French-speaking healthy controls, we assessed AD and DLB patients. Only the action fluency score differed significantly between the two demented groups, with DLB patients performing worse than AD patients. However, a composite action and animal fluency score was found to be more effective for discriminating between these two groups.},\n\tlanguage = {eng},\n\tnumber = {3},\n\tjournal = {Journal of Clinical and Experimental Neuropsychology},\n\tauthor = {Delbeuck, Xavier and Debachy, Brigitte and Pasquier, Florence and Moroni, Christine},\n\tyear = {2013},\n\tpmid = {23379677},\n\tkeywords = {Aged, Aged, 80 and over, Alzheimer Disease, Diagnosis, Differential, Female, Humans, Language, Lewy Body Disease, Male, Middle Aged, Neuropsychological Tests, Speech},\n\tpages = {259--268},\n}\n\n
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\n The objective of the present study was to establish whether performance in an action fluency task is of value in the differential diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). After collecting normative data on performance in an action fluency task and a conventional animal fluency task in a cohort of French-speaking healthy controls, we assessed AD and DLB patients. Only the action fluency score differed significantly between the two demented groups, with DLB patients performing worse than AD patients. However, a composite action and animal fluency score was found to be more effective for discriminating between these two groups.\n
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\n \n\n \n \n \n \n \n A new decision tree combining Abeta 1-42 and p-Tau levels in Alzheimer's diagnosis.\n \n \n \n\n\n \n Bombois, S.; Duhamel, A.; Salleron, J.; Deramecourt, V.; Mackowiak, M.; Deken, V.; Sergeant, N.; Pasquier, F.; Buée, L.; Sablonniére, B.; and Schraen-Maschke, S.\n\n\n \n\n\n\n Current Alzheimer Research, 10(4): 357–364. May 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{bombois_new_2013,\n\ttitle = {A new decision tree combining {Abeta} 1-42 and p-{Tau} levels in {Alzheimer}'s diagnosis},\n\tvolume = {10},\n\tissn = {1875-5828},\n\tdoi = {10.2174/1567205011310040002},\n\tabstract = {The objective of this work was to improve the clinical diagnosis of Alzheimer's disease (AD) by proposing a simple decision tree based on three major biomarkers of AD found in the cerebrospinal fluid (CSF): amyloid peptide Aβ1- 42, total Tau (t-Tau) and Tau phosphorylated at Thr181 (p-Tau). Two consecutive cohorts comprising 548 patients in total were recruited by the Memory and Neurology Clinics at Lille University Hospital (France). These included 293 patients with AD, 171 patients with other dementias and 84 healthy controls. All patients underwent lumbar puncture for the assessment of CSF concentrations of Aβ1-42, t-Tau and p-Tau. International criteria for dementias were used for diagnosis by investigators blind to CSF test results. To identify the combination of biomarkers that best predicted the 3 diagnoses, we used the CHAID decision tree method with the first cohort. Our analysis yielded a two-step decision tree, with a first stratification step based on the Aβ1-42/p-Tau ratio of the CSF, and a second step based on CSF p-Tau concentrations. The second cohort was then used to determine the power (0.618), sensitivity (82\\%) and specificity (81\\%) of this tree in AD diagnosis. These were found to be at least as high as those of other known algorithms based on the three CSF biomarkers, Aβ1-42, t-Tau and p-Tau.For the first time, diagnostic rules for AD based on CSF variables were compared in a single study. Our findings indicate that the measurement of Aβ1-42 and p-Tau levels in the CSF is sufficient to diagnose AD.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Current Alzheimer Research},\n\tauthor = {Bombois, Stéphanie and Duhamel, Alain and Salleron, Julia and Deramecourt, Vincent and Mackowiak, Marie-Anne and Deken, Valérie and Sergeant, Nicholas and Pasquier, Florence and Buée, Luc and Sablonniére, Bernard and Schraen-Maschke, Susanna},\n\tmonth = may,\n\tyear = {2013},\n\tpmid = {23061918},\n\tkeywords = {Adult, Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Cohort Studies, Decision Trees, Female, Humans, Male, Middle Aged, Peptide Fragments, Reference Values, Retrospective Studies, Sensitivity and Specificity, tau Proteins},\n\tpages = {357--364},\n}\n\n
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\n The objective of this work was to improve the clinical diagnosis of Alzheimer's disease (AD) by proposing a simple decision tree based on three major biomarkers of AD found in the cerebrospinal fluid (CSF): amyloid peptide Aβ1- 42, total Tau (t-Tau) and Tau phosphorylated at Thr181 (p-Tau). Two consecutive cohorts comprising 548 patients in total were recruited by the Memory and Neurology Clinics at Lille University Hospital (France). These included 293 patients with AD, 171 patients with other dementias and 84 healthy controls. All patients underwent lumbar puncture for the assessment of CSF concentrations of Aβ1-42, t-Tau and p-Tau. International criteria for dementias were used for diagnosis by investigators blind to CSF test results. To identify the combination of biomarkers that best predicted the 3 diagnoses, we used the CHAID decision tree method with the first cohort. Our analysis yielded a two-step decision tree, with a first stratification step based on the Aβ1-42/p-Tau ratio of the CSF, and a second step based on CSF p-Tau concentrations. The second cohort was then used to determine the power (0.618), sensitivity (82%) and specificity (81%) of this tree in AD diagnosis. These were found to be at least as high as those of other known algorithms based on the three CSF biomarkers, Aβ1-42, t-Tau and p-Tau.For the first time, diagnostic rules for AD based on CSF variables were compared in a single study. Our findings indicate that the measurement of Aβ1-42 and p-Tau levels in the CSF is sufficient to diagnose AD.\n
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\n \n\n \n \n \n \n \n Vascular neuropathology and cognitive decline.\n \n \n \n\n\n \n Deramecourt, V.\n\n\n \n\n\n\n Revue Neurologique, 169(10): 765–771. October 2013.\n \n\n\n\n
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@article{deramecourt_vascular_2013,\n\ttitle = {Vascular neuropathology and cognitive decline},\n\tvolume = {169},\n\tissn = {0035-3787},\n\tdoi = {10.1016/j.neurol.2013.07.008},\n\tabstract = {Cerebrovascular disease is an important cause of cognitive decline and dementia. Despite numerous epidemiological, clinical, neuroimaging and neuropathological studies, the link between cerebrovascular lesions and their impact on cognition and behavior is still a matter of debate. Cerebrovascular lesions are heterogeneous and most descriptive studies distinguish vessel wall modifications, perivascular space modifications, white matter changes, and infarcts as the main features of vascular dementia. However, to date there is still no consensual criteria for the neuropathological diagnosis of vascular or mixed dementia. The diagnosis of these conditions still relies on both clinical and neuropathological expertise.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Revue Neurologique},\n\tauthor = {Deramecourt, V.},\n\tmonth = oct,\n\tyear = {2013},\n\tpmid = {23999025},\n\tkeywords = {Angiopathie amyloïde cérébrale, Arteriolosclerosis, Arteriolosclérose, Cerebral amyloid angiopathy, Cerebrovascular Disorders, Cognition, Cognition Disorders, Dementia, Vascular, Diagnostic Techniques, Neurological, Humans, Lacunar infarct, Lacune, Micro-infarcts, Microinfarctus},\n\tpages = {765--771},\n}\n\n
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\n Cerebrovascular disease is an important cause of cognitive decline and dementia. Despite numerous epidemiological, clinical, neuroimaging and neuropathological studies, the link between cerebrovascular lesions and their impact on cognition and behavior is still a matter of debate. Cerebrovascular lesions are heterogeneous and most descriptive studies distinguish vessel wall modifications, perivascular space modifications, white matter changes, and infarcts as the main features of vascular dementia. However, to date there is still no consensual criteria for the neuropathological diagnosis of vascular or mixed dementia. The diagnosis of these conditions still relies on both clinical and neuropathological expertise.\n
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\n \n\n \n \n \n \n \n New behavioural variant FTD criteria and clinical practice.\n \n \n \n\n\n \n Pasquier, F.\n\n\n \n\n\n\n Revue Neurologique, 169(10): 799–805. October 2013.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pasquier_new_2013,\n\ttitle = {New behavioural variant {FTD} criteria and clinical practice},\n\tvolume = {169},\n\tissn = {0035-3787},\n\tdoi = {10.1016/j.neurol.2013.08.002},\n\tabstract = {Since the first descriptions of circumscribed frontotemporal atrophies, and the first statement published by the Lund and Manchester groups, consensus clinical and pathological criteria for frontotemporal dementia (FTD) have been increasingly refined. The last international behavioural variant FTD criteria (FTDC) (Rascovsky et al., 2011) are the most sensitive, operational and reliable, for the clinical syndrome. Previously exclusion features, like early and severe amnestic syndrome or spatial disorientation, which turn out to be not so rare, are taken into account, as well as imaging, and biomarkers suggestive of other pathologies like Alzheimer's disease. So far, clinical features do not seem very helpful in predicting the underlying histopathology, although there are some clues, mainly related to neurological features (e.g. motor neuron disease, extra-pyramidal symptoms or language disorders), or associated disorders (e.g. Paget disease of bone) or genetics. BvFTD remains a difficult diagnosis at very early stage, which accounts for the delay of diagnosis, especially in late onset, where the frontotemporal atrophy may not be striking. At very young onset, psychiatric diseases must be ruled out. More systematic assessment of social cognition could be helpful. Further biomarkers are expected. Systematic use of recent criteria, for BvFTD and other neurodegenerative diseases especially AD, will contribute to make early and correct diagnoses in excluding or suggesting alternative diagnoses. Post-mortem assessment, with detailed recording of clinical information, is essential to progress.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {Revue Neurologique},\n\tauthor = {Pasquier, F.},\n\tmonth = oct,\n\tyear = {2013},\n\tpmid = {24034691},\n\tkeywords = {Alzheimer's disease, Consensus, Criteria, Critères, Diagnosis, Differential, Diagnostic Techniques, Neurological, Démence fronto-temporale, Frontotemporal Dementia, Frontotemporal dementia, Humans, Maladie d’Alzheimer, Mental Disorders, Practice Guidelines as Topic, Professional Practice},\n\tpages = {799--805},\n}\n\n
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\n Since the first descriptions of circumscribed frontotemporal atrophies, and the first statement published by the Lund and Manchester groups, consensus clinical and pathological criteria for frontotemporal dementia (FTD) have been increasingly refined. The last international behavioural variant FTD criteria (FTDC) (Rascovsky et al., 2011) are the most sensitive, operational and reliable, for the clinical syndrome. Previously exclusion features, like early and severe amnestic syndrome or spatial disorientation, which turn out to be not so rare, are taken into account, as well as imaging, and biomarkers suggestive of other pathologies like Alzheimer's disease. So far, clinical features do not seem very helpful in predicting the underlying histopathology, although there are some clues, mainly related to neurological features (e.g. motor neuron disease, extra-pyramidal symptoms or language disorders), or associated disorders (e.g. Paget disease of bone) or genetics. BvFTD remains a difficult diagnosis at very early stage, which accounts for the delay of diagnosis, especially in late onset, where the frontotemporal atrophy may not be striking. At very young onset, psychiatric diseases must be ruled out. More systematic assessment of social cognition could be helpful. Further biomarkers are expected. Systematic use of recent criteria, for BvFTD and other neurodegenerative diseases especially AD, will contribute to make early and correct diagnoses in excluding or suggesting alternative diagnoses. Post-mortem assessment, with detailed recording of clinical information, is essential to progress.\n
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\n  \n 2012\n \n \n (8)\n \n \n
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\n \n\n \n \n \n \n \n Staging and natural history of cerebrovascular pathology in dementia.\n \n \n \n\n\n \n Deramecourt, V; Slade, J Y; Oakley, A E; Perry, R H; and Ince, P G\n\n\n \n\n\n\n ,9. 2012.\n \n\n\n\n
\n\n\n\n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{deramecourt_staging_2012,\n\ttitle = {Staging and natural history of cerebrovascular pathology in dementia},\n\tabstract = {Objective: Most pathologic studies indicate that significant vascular changes are found in the J.Y. Slade, BSc majority of elderly persons, either alone or in association with neurodegenerative processes such A.E. Oakley, MBiol as Alzheimer disease (AD) or dementia with Lewy bodies (DLB). Cumulative burden of cerebrovasR.H. Perry, FRCPath cular lesions can explain cognitive decline described as vascular cognitive impairment, but beP.G. Ince, FRCPath cause there is a lack of consensus in the best way to quantify vascular pathology, the relationship C.-A. Maurage, MD, between cognitive decline and cerebrovascular disease remains uncertain. We developed a rating PhD scheme for cerebrovascular lesions using postmortem brains from patients with dementia from 2 Seeed R.N. Kalaria, FRCPath European tertiary care memory clinics. Correspondence \\& reprint requests to Dr. Kalaria: r.n.kalaria@ncl.ac.uk\nMethods: A total of 135 brains with a neuropathologic diagnosis of vascular dementia (VaD) (n ϭ 26), AD ϩ VaD (n ϭ 39), DLB ϩ VaD (n ϭ 21), AD ϩ DLB ϩ VaD (n ϭ 9), AD (n ϭ 19), and DLB (n ϭ 21) were investigated in this study. Cerebrovascular lesions were rated on large sections from the hippocampus, the temporal lobe, the frontal lobe, and basal ganglia.\nResults: In patients with dementia, vessel wall modifications such as arteriolosclerosis or amyloid angiopathy are the most common and presumably the earliest changes. Modifications in perivascular spaces and myelin loss are the next most common. Lacunar or regional infarcts may occur as a consequence of an independent process or in the final phase of small vessel diseases.\nConclusion: A staging system based on this conceptual model of cerebrovascular pathology could enable the neuropathologic quantification of the cerebrovascular burden in dementia. Further studies are needed to determine whether this system can be used in large-scale studies to understand clinical–cerebrovascular pathologic correlations. Neurology® 2012;78:1–1},\n\tlanguage = {en},\n\tauthor = {Deramecourt, V and Slade, J Y and Oakley, A E and Perry, R H and Ince, P G},\n\tyear = {2012},\n\tkeywords = {Aged, Aged, 80 and over, Brain, Cerebrovascular Disorders, Dementia, Female, Humans, Male},\n\tpages = {9},\n}\n\n
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\n Objective: Most pathologic studies indicate that significant vascular changes are found in the J.Y. Slade, BSc majority of elderly persons, either alone or in association with neurodegenerative processes such A.E. Oakley, MBiol as Alzheimer disease (AD) or dementia with Lewy bodies (DLB). Cumulative burden of cerebrovasR.H. Perry, FRCPath cular lesions can explain cognitive decline described as vascular cognitive impairment, but beP.G. Ince, FRCPath cause there is a lack of consensus in the best way to quantify vascular pathology, the relationship C.-A. Maurage, MD, between cognitive decline and cerebrovascular disease remains uncertain. We developed a rating PhD scheme for cerebrovascular lesions using postmortem brains from patients with dementia from 2 Seeed R.N. Kalaria, FRCPath European tertiary care memory clinics. Correspondence & reprint requests to Dr. Kalaria: r.n.kalaria@ncl.ac.uk Methods: A total of 135 brains with a neuropathologic diagnosis of vascular dementia (VaD) (n ϭ 26), AD ϩ VaD (n ϭ 39), DLB ϩ VaD (n ϭ 21), AD ϩ DLB ϩ VaD (n ϭ 9), AD (n ϭ 19), and DLB (n ϭ 21) were investigated in this study. Cerebrovascular lesions were rated on large sections from the hippocampus, the temporal lobe, the frontal lobe, and basal ganglia. Results: In patients with dementia, vessel wall modifications such as arteriolosclerosis or amyloid angiopathy are the most common and presumably the earliest changes. Modifications in perivascular spaces and myelin loss are the next most common. Lacunar or regional infarcts may occur as a consequence of an independent process or in the final phase of small vessel diseases. Conclusion: A staging system based on this conceptual model of cerebrovascular pathology could enable the neuropathologic quantification of the cerebrovascular burden in dementia. Further studies are needed to determine whether this system can be used in large-scale studies to understand clinical–cerebrovascular pathologic correlations. Neurology® 2012;78:1–1\n
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\n \n\n \n \n \n \n \n Can the treatment of vascular risk factors slow cognitive decline in Alzheimer's disease patients?.\n \n \n \n\n\n \n Richard, F.; and Pasquier, F.\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 32(3): 765–772. 2012.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{richard_can_2012,\n\ttitle = {Can the treatment of vascular risk factors slow cognitive decline in {Alzheimer}'s disease patients?},\n\tvolume = {32},\n\tissn = {1875-8908},\n\tdoi = {10.3233/JAD-2012-121012},\n\tabstract = {Dementia is a widespread disorder with major medical, economic and societal costs. Controlling vascular conditions could be one way of delaying the progression of Alzheimer's disease (AD). In fact, vascular risk factors are implicated in AD occurrence. However, it has not been clearly determined whether these vascular factors also affect disease progression itself and thus whether controlling vascular conditions can slow this progression. The treatment of vascular risk factors could have an impact on disease progression by slowing the development of the vascular component. In the present article, we review the potential value of managing hypertension, diabetes, hypercholesterolemia or global vascular risk factors in AD patients.},\n\tlanguage = {eng},\n\tnumber = {3},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Richard, Florence and Pasquier, Florence},\n\tyear = {2012},\n\tpmid = {22886010},\n\tkeywords = {Alzheimer Disease, Animals, Cerebrovascular Disorders, Cognition Disorders, Diabetes Mellitus, Disease Progression, Humans, Hypercholesterolemia, Risk Factors, Treatment Outcome},\n\tpages = {765--772},\n}\n\n
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\n Dementia is a widespread disorder with major medical, economic and societal costs. Controlling vascular conditions could be one way of delaying the progression of Alzheimer's disease (AD). In fact, vascular risk factors are implicated in AD occurrence. However, it has not been clearly determined whether these vascular factors also affect disease progression itself and thus whether controlling vascular conditions can slow this progression. The treatment of vascular risk factors could have an impact on disease progression by slowing the development of the vascular component. In the present article, we review the potential value of managing hypertension, diabetes, hypercholesterolemia or global vascular risk factors in AD patients.\n
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\n \n\n \n \n \n \n \n My belief or yours? Differential theory of mind deficits in frontotemporal dementia and Alzheimer's disease.\n \n \n \n\n\n \n Le Bouc, R.; Lenfant, P.; Delbeuck, X.; Ravasi, L.; Lebert, F.; Semah, F.; and Pasquier, F.\n\n\n \n\n\n\n Brain: A Journal of Neurology, 135(Pt 10): 3026–3038. October 2012.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{le_bouc_my_2012,\n\ttitle = {My belief or yours? {Differential} theory of mind deficits in frontotemporal dementia and {Alzheimer}'s disease},\n\tvolume = {135},\n\tissn = {1460-2156},\n\tshorttitle = {My belief or yours?},\n\tdoi = {10.1093/brain/aws237},\n\tabstract = {Theory of mind reasoning-the ability to understand someone else's mental states, such as beliefs, intentions and desires-is crucial in social interaction. It has been suggested that a theory of mind deficit may account for some of the abnormalities in interpersonal behaviour that characterize patients affected by behavioural variant frontotemporal dementia. However, there are conflicting reports as to whether understanding someone else's mind is a key difference between behavioural variant frontotemporal dementia and other neurodegenerative conditions such as Alzheimer's disease. Literature data on the relationship between theory of mind abilities and executive functions are also contradictory. These disparities may be due to underestimation of the fractionation within theory of mind components. A recent theoretical framework suggests that taking someone else's mental perspective requires two distinct processes: inferring someone else's belief and inhibiting one's own belief, with involvement of the temporoparietal and right frontal cortices, respectively. Therefore, we performed a neuropsychological and neuroimaging study to investigate the hypothesis whereby distinct cognitive deficits could impair theory of mind reasoning in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia. We used a three-option false belief task to assess theory of mind components in 11 patients with behavioural variant frontotemporal dementia, 12 patients with Alzheimer's disease and 20 healthy elderly control subjects. The patients with behavioural variant frontotemporal dementia and those with Alzheimer's disease were matched for age, gender, education and global cognitive impairment. [(18)F]-fluorodeoxyglucose-positron emission tomography imaging was used to investigate neural correlates of theory of mind reasoning deficits. Performance in the three-option false belief task revealed differential impairments in the components of theory of mind reasoning; patients with Alzheimer's disease had a predominant deficit in inferring someone else's belief, whereas patients with behavioural variant frontotemporal dementia were selectively impaired in inhibiting their own mental perspective. Moreover, inhibiting one's own perspective was strongly correlated with inhibition in a Stroop task but not with other subprocesses of executive functions. This finding suggests that self-perspective inhibition may depend on cognitive processes that are not specific to the social domain. Last, the severity of the deficit in inferring someone else's beliefs correlated significantly over all subjects with hypometabolism in the left temporoparietal junction, whereas the severity of the deficit in self-perspective inhibition correlated significantly with hypometabolism in the right lateral prefrontal cortex. In conclusion, our findings provided clinical and imaging evidence to support differential deficits in two components of theory of mind reasoning (subserved by distinct brain regions) in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia.},\n\tlanguage = {eng},\n\tnumber = {Pt 10},\n\tjournal = {Brain: A Journal of Neurology},\n\tauthor = {Le Bouc, Raphaël and Lenfant, Pierre and Delbeuck, Xavier and Ravasi, Laura and Lebert, Florence and Semah, Franck and Pasquier, Florence},\n\tmonth = oct,\n\tyear = {2012},\n\tpmid = {23065791},\n\tkeywords = {Aged, Alzheimer Disease, Cerebral Cortex, Fluorodeoxyglucose F18, Frontotemporal Dementia, Humans, Male, Middle Aged, Neuropsychological Tests, Theory of Mind},\n\tpages = {3026--3038},\n}\n\n
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\n Theory of mind reasoning-the ability to understand someone else's mental states, such as beliefs, intentions and desires-is crucial in social interaction. It has been suggested that a theory of mind deficit may account for some of the abnormalities in interpersonal behaviour that characterize patients affected by behavioural variant frontotemporal dementia. However, there are conflicting reports as to whether understanding someone else's mind is a key difference between behavioural variant frontotemporal dementia and other neurodegenerative conditions such as Alzheimer's disease. Literature data on the relationship between theory of mind abilities and executive functions are also contradictory. These disparities may be due to underestimation of the fractionation within theory of mind components. A recent theoretical framework suggests that taking someone else's mental perspective requires two distinct processes: inferring someone else's belief and inhibiting one's own belief, with involvement of the temporoparietal and right frontal cortices, respectively. Therefore, we performed a neuropsychological and neuroimaging study to investigate the hypothesis whereby distinct cognitive deficits could impair theory of mind reasoning in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia. We used a three-option false belief task to assess theory of mind components in 11 patients with behavioural variant frontotemporal dementia, 12 patients with Alzheimer's disease and 20 healthy elderly control subjects. The patients with behavioural variant frontotemporal dementia and those with Alzheimer's disease were matched for age, gender, education and global cognitive impairment. [(18)F]-fluorodeoxyglucose-positron emission tomography imaging was used to investigate neural correlates of theory of mind reasoning deficits. Performance in the three-option false belief task revealed differential impairments in the components of theory of mind reasoning; patients with Alzheimer's disease had a predominant deficit in inferring someone else's belief, whereas patients with behavioural variant frontotemporal dementia were selectively impaired in inhibiting their own mental perspective. Moreover, inhibiting one's own perspective was strongly correlated with inhibition in a Stroop task but not with other subprocesses of executive functions. This finding suggests that self-perspective inhibition may depend on cognitive processes that are not specific to the social domain. Last, the severity of the deficit in inferring someone else's beliefs correlated significantly over all subjects with hypometabolism in the left temporoparietal junction, whereas the severity of the deficit in self-perspective inhibition correlated significantly with hypometabolism in the right lateral prefrontal cortex. In conclusion, our findings provided clinical and imaging evidence to support differential deficits in two components of theory of mind reasoning (subserved by distinct brain regions) in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia.\n
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\n \n\n \n \n \n \n \n Clinical, neuropathological, and biochemical characterization of the novel tau mutation P332S.\n \n \n \n\n\n \n Deramecourt, V.; Lebert, F.; Maurage, C.; Fernandez-Gomez, F.; Dujardin, S.; Colin, M.; Sergeant, N.; Buée-Scherrer, V.; Clot, F.; Ber, I. L.; Brice, A.; Pasquier, F.; and Buée, L.\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 31(4): 741–749. 2012.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{deramecourt_clinical_2012,\n\ttitle = {Clinical, neuropathological, and biochemical characterization of the novel tau mutation {P332S}},\n\tvolume = {31},\n\tissn = {1875-8908},\n\tdoi = {10.3233/JAD-2012-120160},\n\tabstract = {MAPT mutations cause autosomal dominant frontotemporal lobar degeneration. These diseases are characterized by considerable heterogeneity in their clinical, neuropathological, and biochemical presentations. We describe the full characterization of a family with autosomal dominant frontotemporal lobar degeneration caused by a novel MAPT mutation. Clinical, imaging, neuropathological, and biochemical data are presented. The proband was a woman who died at 85 years old, 25 years after the onset of a slowly progressive and isolated anarthria and opercular syndrome. The pathological examination of her brain showed marked atrophy of primary motor and premotor cortices, associated with predominant neuronal tau-positive lesions mimicking Pick bodies. At the biochemical level, the six tau isoforms aggregate to display a pathological triplet at 60, 64, and 69 kDa. Two of her sons presented at 48 and 50 years old with a right temporal variant of frontotemporal degeneration characterized by severe prosopagnosia, semantic impairment, and behavioral modifications. In these three patients, the molecular analysis of MAPT showed the c.1945C{\\textgreater}T mutation on exon 11 resulting in the P332S substitution in tau sequence. This mutation changes the PGGG motif of the third repeat domain of the protein and therefore reduces the ability of tau to bind microtubule. From a clinical point of view, this mutation is associated with considerable intrafamilial phenotypic variation.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Deramecourt, Vincent and Lebert, Florence and Maurage, Claude-Alain and Fernandez-Gomez, Francisco-Jose and Dujardin, Simon and Colin, Morvane and Sergeant, Nicolas and Buée-Scherrer, Valérie and Clot, Fabienne and Ber, Isabelle Le and Brice, Alexis and Pasquier, Florence and Buée, Luc},\n\tyear = {2012},\n\tpmid = {22699846},\n\tkeywords = {Aged, 80 and over, Female, Follow-Up Studies, Frontotemporal Lobar Degeneration, Genetic Variation, HEK293 Cells, Humans, Male, Middle Aged, Mutation, Pedigree, Phenotype, tau Proteins},\n\tpages = {741--749},\n}\n\n
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\n MAPT mutations cause autosomal dominant frontotemporal lobar degeneration. These diseases are characterized by considerable heterogeneity in their clinical, neuropathological, and biochemical presentations. We describe the full characterization of a family with autosomal dominant frontotemporal lobar degeneration caused by a novel MAPT mutation. Clinical, imaging, neuropathological, and biochemical data are presented. The proband was a woman who died at 85 years old, 25 years after the onset of a slowly progressive and isolated anarthria and opercular syndrome. The pathological examination of her brain showed marked atrophy of primary motor and premotor cortices, associated with predominant neuronal tau-positive lesions mimicking Pick bodies. At the biochemical level, the six tau isoforms aggregate to display a pathological triplet at 60, 64, and 69 kDa. Two of her sons presented at 48 and 50 years old with a right temporal variant of frontotemporal degeneration characterized by severe prosopagnosia, semantic impairment, and behavioral modifications. In these three patients, the molecular analysis of MAPT showed the c.1945C\\textgreaterT mutation on exon 11 resulting in the P332S substitution in tau sequence. This mutation changes the PGGG motif of the third repeat domain of the protein and therefore reduces the ability of tau to bind microtubule. From a clinical point of view, this mutation is associated with considerable intrafamilial phenotypic variation.\n
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\n \n\n \n \n \n \n \n Contribution of single photon emission computed tomography to the differential diagnosis of dementia in a memory clinic.\n \n \n \n\n\n \n Rollin-Sillaire, A.; Bombois, S.; Deramecourt, V.; Steinert-Emptaz, A.; Salleron, J.; Morvan, J.; Maurage, C.; Steinling, M.; and Pasquier, F.\n\n\n \n\n\n\n Journal of Alzheimer's disease: JAD, 30(4): 833–845. 2012.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{rollin-sillaire_contribution_2012,\n\ttitle = {Contribution of single photon emission computed tomography to the differential diagnosis of dementia in a memory clinic},\n\tvolume = {30},\n\tissn = {1875-8908},\n\tdoi = {10.3233/JAD-2012-111067},\n\tabstract = {To evaluate the contribution of single photon emission computed tomography (SPECT) to the differential diagnosis of dementia, we studied 48 consecutive patients (median age: 63) with a degenerative or vascular dementia, a 99mTc-HMPAO SPECT imaging, and a diagnostic confirmation (autopsy or genetic mutation). The SPECT scans were visually rated by two nuclear medicine physicians (first blinded to the clinical data, then with the data). Comparisons between clinical diagnoses and/or SPECT imaging and neuropathology were performed. At the time of SPECT was performed, the clinical diagnosis of Alzheimer's disease (AD) sensitivity was 83\\%, specificity was 76\\%, and diagnostic accuracy was 79\\%. The blinded SPECT sensitivity was 57\\%, specificity 92\\%, and diagnostic accuracy 75\\%. The SPECT associated with clinical data sensitivity was 65\\%, specificity 84\\%, and accuracy 75\\%. The clinical diagnosis of frontotemporal-lobar degeneration (FTLD), progressive supranuclear palsy (PSP), and corticobasal degeneration syndrome (CBDs) sensitivity was 83\\%, specificity 87\\%, and accuracy 85\\%. The blinded SPECT sensitivity was 50\\%, specificity 97\\%, and accuracy 79\\%. The SPECT associated with clinical data sensitivity was 61\\%, specificity was 93\\%, and accuracy 81\\%. Whenever the blinded SPECT interpretation agreed with the clinical diagnosis of AD and FTLD/PSP/CBDs, the condition was confirmed by neuropathological assessment in all cases. Compared with clinical diagnosis alone, SPECT imaging improved the specificity of the etiological diagnosis in degenerative dementia, although its sensitivity was not as good as that of clinical diagnosis. For AD and FTLD/PSP/CBDs, agreement between the clinical and SPECT-based diagnoses was always confirmed by neuropathological assessment.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of Alzheimer's disease: JAD},\n\tauthor = {Rollin-Sillaire, Adeline and Bombois, Stéphanie and Deramecourt, Vincent and Steinert-Emptaz, Aline and Salleron, Julia and Morvan, Julie and Maurage, Claude-Alain and Steinling, Marc and Pasquier, Florence},\n\tyear = {2012},\n\tpmid = {22460325},\n\tkeywords = {Aged, Dementia, Diagnosis, Differential, Female, Humans, Longitudinal Studies, Male, Memory, Middle Aged, Outpatient Clinics, Hospital, Single-Blind Method, Tomography, Emission-Computed, Single-Photon},\n\tpages = {833--845},\n}\n\n
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\n To evaluate the contribution of single photon emission computed tomography (SPECT) to the differential diagnosis of dementia, we studied 48 consecutive patients (median age: 63) with a degenerative or vascular dementia, a 99mTc-HMPAO SPECT imaging, and a diagnostic confirmation (autopsy or genetic mutation). The SPECT scans were visually rated by two nuclear medicine physicians (first blinded to the clinical data, then with the data). Comparisons between clinical diagnoses and/or SPECT imaging and neuropathology were performed. At the time of SPECT was performed, the clinical diagnosis of Alzheimer's disease (AD) sensitivity was 83%, specificity was 76%, and diagnostic accuracy was 79%. The blinded SPECT sensitivity was 57%, specificity 92%, and diagnostic accuracy 75%. The SPECT associated with clinical data sensitivity was 65%, specificity 84%, and accuracy 75%. The clinical diagnosis of frontotemporal-lobar degeneration (FTLD), progressive supranuclear palsy (PSP), and corticobasal degeneration syndrome (CBDs) sensitivity was 83%, specificity 87%, and accuracy 85%. The blinded SPECT sensitivity was 50%, specificity 97%, and accuracy 79%. The SPECT associated with clinical data sensitivity was 61%, specificity was 93%, and accuracy 81%. Whenever the blinded SPECT interpretation agreed with the clinical diagnosis of AD and FTLD/PSP/CBDs, the condition was confirmed by neuropathological assessment in all cases. Compared with clinical diagnosis alone, SPECT imaging improved the specificity of the etiological diagnosis in degenerative dementia, although its sensitivity was not as good as that of clinical diagnosis. For AD and FTLD/PSP/CBDs, agreement between the clinical and SPECT-based diagnoses was always confirmed by neuropathological assessment.\n
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\n \n\n \n \n \n \n \n [From Pick's disease to frontotemporal dementia].\n \n \n \n\n\n \n Pasquier, F.; Deramecourt, V.; and Lebert, F.\n\n\n \n\n\n\n Bulletin De l'Academie Nationale De Medecine, 196(2): 431–442; discussion 442–443. February 2012.\n \n\n\n\n
\n\n\n\n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{pasquier_picks_2012,\n\ttitle = {[{From} {Pick}'s disease to frontotemporal dementia]},\n\tvolume = {196},\n\tissn = {0001-4079},\n\tabstract = {Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinicalfeatures depend on the location of the degenerative process. In the last 20 years, increasingly specific and sensitive operational criteria have been established. Ongoing neuropathological and genetic studies have highlighted overlaps between FTD, motor neuron disease, and atypical parkinsonian syndromes (supranuclear palsy, corticobasal degeneration). They have also provided a better knowledge of the pathophysiology of FTD, and new specific therapeutic targets. These dementias, which usually occur before the age of 65 years, are now better recognized but are still underdiagnosed and often initially mistaken for psychiatric illnesses. Healthcare professionals managing these patients must therefore be better informed Serotonergic agents provide a symptomatic improvement, but environmental adaptation, prevention of language and swallowing difficulties, and information and support for the family and caregivers remain essential.},\n\tlanguage = {fre},\n\tnumber = {2},\n\tjournal = {Bulletin De l'Academie Nationale De Medecine},\n\tauthor = {Pasquier, Florence and Deramecourt, Vincent and Lebert, Florence},\n\tmonth = feb,\n\tyear = {2012},\n\tpmid = {23420961},\n\tkeywords = {Behavioral Symptoms, Diagnosis, Differential, Frontotemporal Dementia, Humans, Pick Disease of the Brain},\n\tpages = {431--442; discussion 442--443},\n}\n\n
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\n Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinicalfeatures depend on the location of the degenerative process. In the last 20 years, increasingly specific and sensitive operational criteria have been established. Ongoing neuropathological and genetic studies have highlighted overlaps between FTD, motor neuron disease, and atypical parkinsonian syndromes (supranuclear palsy, corticobasal degeneration). They have also provided a better knowledge of the pathophysiology of FTD, and new specific therapeutic targets. These dementias, which usually occur before the age of 65 years, are now better recognized but are still underdiagnosed and often initially mistaken for psychiatric illnesses. Healthcare professionals managing these patients must therefore be better informed Serotonergic agents provide a symptomatic improvement, but environmental adaptation, prevention of language and swallowing difficulties, and information and support for the family and caregivers remain essential.\n
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\n \n\n \n \n \n \n \n [Alzheimer's disease and related disorders: specificity of young onset patients, including ethical aspects].\n \n \n \n\n\n \n Lebert, F.; Boitte, P.; de Bouvet, A.; and Pasquier, F.\n\n\n \n\n\n\n Geriatrie Et Psychologie Neuropsychiatrie Du Vieillissement, 10(1): 65–72. March 2012.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n  \n \n\n \n link\n  \n \n\n bibtex\n \n\n \n  \n \n abstract \n \n\n \n  \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n
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@article{lebert_alzheimers_2012,\n\ttitle = {[{Alzheimer}'s disease and related disorders: specificity of young onset patients, including ethical aspects]},\n\tvolume = {10},\n\tissn = {2115-8789},\n\tshorttitle = {[{Alzheimer}'s disease and related disorders},\n\tdoi = {10.1684/pnv.2012.0316},\n\tabstract = {The number of patients with young onset dementia (YOD) (that is before age 65) is estimated at 32,000 in France, and 5000 with onset dementia before 60 years. These patients differ from older ones by the greater number of rares causes (29\\%), heterogeneity of the presentation among the usual diseases, such as non-amnestic phenotypes of Alzheimer's disease, high frequency of frontal symptoms, and possible genetic origin. These aspects must be taken into account for the diagnosis, often more difficult than in older ones because patients have a little knowledge of the YOD, excepted in the genetics forms. YOD patients can still work or drive a car, and we should choose between the respect for autonomy and the security for the patient and their carers. YOD patients can be more often included in pharmacological trials because they have lower associated disorders. Individual non-pharmacological treatment should be priviledged because they don't easily accept collective activities with other patients over 60 years of age. Excepted for the very young patients (onset before 45), the survival is longer than in late onset dementia, with sometimes severe behavioral problems related to frontal syndrome. In France, the caregiving at home has been improved since the possibility for the YOD patients to receive a financial assistance reserved for the disabled patients, but admission to a nursing home before 60 is very difficult and increases the caregiver burden and perception of unfairness. There is a discrimination between young or older demented patients related to the great difficulty to meet the needs of younger patients, due to the rigidity of the medical and social systems. The presentation of a limited offer for the YOD patients must initiate reflections on our capacities to respect the autonomy and the dignity of the Alzheimer's patients regardless of age.},\n\tlanguage = {fre},\n\tnumber = {1},\n\tjournal = {Geriatrie Et Psychologie Neuropsychiatrie Du Vieillissement},\n\tauthor = {Lebert, Florence and Boitte, Pierre and de Bouvet, Armelle and Pasquier, Florence},\n\tmonth = mar,\n\tyear = {2012},\n\tpmid = {22414401},\n\tkeywords = {Age Factors, Aged, Alzheimer Disease, Caregivers, Cost of Illness, Dementia, Vascular, Eligibility Determination, Ethics, Medical, Female, France, Frontotemporal Dementia, Health Services Accessibility, Homes for the Aged, Humans, Lewy Body Disease, Male, Middle Aged, National Health Programs, Nursing Homes, Prevalence, Public Policy, Risk Factors, Social Security, Survival Rate},\n\tpages = {65--72},\n}\n\n
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\n The number of patients with young onset dementia (YOD) (that is before age 65) is estimated at 32,000 in France, and 5000 with onset dementia before 60 years. These patients differ from older ones by the greater number of rares causes (29%), heterogeneity of the presentation among the usual diseases, such as non-amnestic phenotypes of Alzheimer's disease, high frequency of frontal symptoms, and possible genetic origin. These aspects must be taken into account for the diagnosis, often more difficult than in older ones because patients have a little knowledge of the YOD, excepted in the genetics forms. YOD patients can still work or drive a car, and we should choose between the respect for autonomy and the security for the patient and their carers. YOD patients can be more often included in pharmacological trials because they have lower associated disorders. Individual non-pharmacological treatment should be priviledged because they don't easily accept collective activities with other patients over 60 years of age. Excepted for the very young patients (onset before 45), the survival is longer than in late onset dementia, with sometimes severe behavioral problems related to frontal syndrome. In France, the caregiving at home has been improved since the possibility for the YOD patients to receive a financial assistance reserved for the disabled patients, but admission to a nursing home before 60 is very difficult and increases the caregiver burden and perception of unfairness. There is a discrimination between young or older demented patients related to the great difficulty to meet the needs of younger patients, due to the rigidity of the medical and social systems. The presentation of a limited offer for the YOD patients must initiate reflections on our capacities to respect the autonomy and the dignity of the Alzheimer's patients regardless of age.\n
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\n \n\n \n \n \n \n \n Detection of microbleeds in post-mortem brains of patients with frontotemporal lobar degeneration: a 7.0-Tesla magnetic resonance imaging study with neuropathological correlates.\n \n \n \n\n\n \n De Reuck, J.; Deramecourt, V.; Cordonnier, C.; Auger, F.; Durieux, N.; Bordet, R.; Maurage, C. A.; Leys, D.; and Pasquier, F.\n\n\n \n\n\n\n European Journal of Neurology, 19(10): 1355–1360. October 2012.\n \n\n\n\n
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@article{de_reuck_detection_2012,\n\ttitle = {Detection of microbleeds in post-mortem brains of patients with frontotemporal lobar degeneration: a 7.0-{Tesla} magnetic resonance imaging study with neuropathological correlates},\n\tvolume = {19},\n\tissn = {1468-1331},\n\tshorttitle = {Detection of microbleeds in post-mortem brains of patients with frontotemporal lobar degeneration},\n\tdoi = {10.1111/j.1468-1331.2012.03776.x},\n\tabstract = {BACKGROUND: Microbleeds (MBs) are frequently detected in brains of patients with Alzheimer dementia and rare in those with frontotemporal lobar degeneration (FTLD). This study investigates for the first time the topographic distribution of MBs on a T2*-weighted gradient-echo 7.0-T magnetic resonance imaging (MRI) in post-mortem FTLD brains.\nPATIENTS AND METHODS: The neuropathological and MRI findings in 12 FTLD brains were compared with eight age-matched controls. The presence of cerebrovascular lesions was evaluated on a coronal section of a cerebral hemisphere at the level of the mamillary body and on a horizontal section through pons and cerebellum. On MRI, the distribution and the number of cortical focal signal intensity losses, representing MBs, were assessed on coronal sections at the frontal, the central and the occipital level of a cerebral hemisphere.\nRESULTS: Overall, cerebrovascular lesions were rare. Only white matter damage was significantly more severe in FTLD brains compared with controls (P = 0.03). On MRI, MBs were only significantly prevalent in the deep cortical layers (P {\\textless} 0.01) and borderline increased in the middle cortical layers (P = 0.07) of the frontal section.\nCONCLUSIONS: Cerebrovascular lesions are rare in FTLD. The white matter damage has to be considered as part of the neurodegenerative process. MBs prevail in the frontal regions with the most severe neuronal damage and probably represent associated disruption of the blood-brain barrier.},\n\tlanguage = {eng},\n\tnumber = {10},\n\tjournal = {European Journal of Neurology},\n\tauthor = {De Reuck, J. and Deramecourt, V. and Cordonnier, C. and Auger, F. and Durieux, N. and Bordet, R. and Maurage, C. A. and Leys, D. and Pasquier, F.},\n\tmonth = oct,\n\tyear = {2012},\n\tpmid = {22642502},\n\tkeywords = {Adult, Age of Onset, Aged, Aged, 80 and over, Autopsy, Blood-Brain Barrier, Brain, Cerebral Hemorrhage, Female, Frontotemporal Lobar Degeneration, Humans, Magnetic Resonance Imaging, Male, Middle Aged},\n\tpages = {1355--1360},\n}\n\n
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\n BACKGROUND: Microbleeds (MBs) are frequently detected in brains of patients with Alzheimer dementia and rare in those with frontotemporal lobar degeneration (FTLD). This study investigates for the first time the topographic distribution of MBs on a T2*-weighted gradient-echo 7.0-T magnetic resonance imaging (MRI) in post-mortem FTLD brains. PATIENTS AND METHODS: The neuropathological and MRI findings in 12 FTLD brains were compared with eight age-matched controls. The presence of cerebrovascular lesions was evaluated on a coronal section of a cerebral hemisphere at the level of the mamillary body and on a horizontal section through pons and cerebellum. On MRI, the distribution and the number of cortical focal signal intensity losses, representing MBs, were assessed on coronal sections at the frontal, the central and the occipital level of a cerebral hemisphere. RESULTS: Overall, cerebrovascular lesions were rare. Only white matter damage was significantly more severe in FTLD brains compared with controls (P = 0.03). On MRI, MBs were only significantly prevalent in the deep cortical layers (P \\textless 0.01) and borderline increased in the middle cortical layers (P = 0.07) of the frontal section. CONCLUSIONS: Cerebrovascular lesions are rare in FTLD. The white matter damage has to be considered as part of the neurodegenerative process. MBs prevail in the frontal regions with the most severe neuronal damage and probably represent associated disruption of the blood-brain barrier.\n
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