@article{ hommet_neuroinflammation_2014,
  title = {Neuroinflammation and β amyloid deposition in {Alzheimer}'s disease: in vivo quantification with molecular imaging},
  volume = {37},
  issn = {1421-9824},
  shorttitle = {Neuroinflammation and β amyloid deposition in {Alzheimer}'s disease},
  doi = {10.1159/000354363},
  abstract = {BACKGROUND/AIMS: Neuroinflammation plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Its relationship with underlying β amyloid deposition remains unclear. In vivo visualization of microglial activation has become possible with the development of molecular imaging ligands when used with positron emission tomography (PET). The translocator protein (TSPO) is upregulated during neuroinflammation. Consequently, targeting TSPO with radiolabeled ligands for PET is an attractive biomarker for neuroinflammation.
METHODS: A review of the research literature on PET imaging which studied in vivo neuroinflammation in AD subjects and its relationship with amyloid load was performed, including papers published between 2001 and 2012.
RESULTS: Six studies were included using either [(11)C]PK-11195 or another non-TSPO radioligand that binds to the monoaminooxidase B. All the studies evaluated amyloid load with [(11)C]PIB. Microglial activation and astrocytosis are potentially early phenomena in AD. However, the individual levels of amyloid deposition and microglial activation were not correlated.
CONCLUSION: Noninvasive in vivo molecular imaging to visualize neuroinflammation in AD may contribute to our understanding of the kinetics of neuroinflammation and its relationship to the hallmarks of the disease. Both are important for the development of future therapeutic modalities and for quantifying the efficacy of future disease-modifying treatments.},
  language = {eng},
  number = {1-2},
  journal = {Dementia and Geriatric Cognitive Disorders},
  author = {Hommet, C. and Mondon, K. and Camus, V. and Ribeiro, M. J. and Beaufils, E. and Arlicot, N. and Corcia, P. and Paccalin, M. and Minier, F. and Gosselin, T. and Page, G. and Guilloteau, D. and Chalon, S.},
  year = {2014},
  pmid = {24107621},
  keywords = {Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Benzothiazoles, Brain, Humans, Inflammation, Isoquinolines, Mitochondrial ADP, ATP Translocases, Molecular Imaging, Monoamine Oxidase, Positron-Emission Tomography, Radiopharmaceuticals, tau Proteins},
  pages = {1--18}
}

{"_id":"PdXPXNffbbMTmojff","authorIDs":[],"author_short":["Hommet, C.","Mondon, K.","Camus, V.","Ribeiro, M.<nbsp>J.","Beaufils, E.","Arlicot, N.","Corcia, P.","Paccalin, M.","Minier, F.","Gosselin, T.","Page, G.","Guilloteau, D.","Chalon, S."],"bibbaseid":"hommet-mondon-camus-ribeiro-beaufils-arlicot-corcia-paccalin-minier-gosselin-page-guilloteau-chalon-neuroinflammationandamyloiddepositioninalzheimersdiseaseinvivoquantificationwithmolecularimaging-2014","bibdata":{"abstract":"BACKGROUND/AIMS: Neuroinflammation plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Its relationship with underlying β amyloid deposition remains unclear. In vivo visualization of microglial activation has become possible with the development of molecular imaging ligands when used with positron emission tomography (PET). The translocator protein (TSPO) is upregulated during neuroinflammation. Consequently, targeting TSPO with radiolabeled ligands for PET is an attractive biomarker for neuroinflammation. METHODS: A review of the research literature on PET imaging which studied in vivo neuroinflammation in AD subjects and its relationship with amyloid load was performed, including papers published between 2001 and 2012. RESULTS: Six studies were included using either [(11)C]PK-11195 or another non-TSPO radioligand that binds to the monoaminooxidase B. All the studies evaluated amyloid load with [(11)C]PIB. Microglial activation and astrocytosis are potentially early phenomena in AD. However, the individual levels of amyloid deposition and microglial activation were not correlated. CONCLUSION: Noninvasive in vivo molecular imaging to visualize neuroinflammation in AD may contribute to our understanding of the kinetics of neuroinflammation and its relationship to the hallmarks of the disease. Both are important for the development of future therapeutic modalities and for quantifying the efficacy of future disease-modifying treatments.","author":["Hommet, C.","Mondon, K.","Camus, V.","Ribeiro, M. J.","Beaufils, E.","Arlicot, N.","Corcia, P.","Paccalin, M.","Minier, F.","Gosselin, T.","Page, G.","Guilloteau, D.","Chalon, S."],"author_short":["Hommet, C.","Mondon, K.","Camus, V.","Ribeiro, M.<nbsp>J.","Beaufils, E.","Arlicot, N.","Corcia, P.","Paccalin, M.","Minier, F.","Gosselin, T.","Page, G.","Guilloteau, D.","Chalon, S."],"bibtex":"@article{ hommet_neuroinflammation_2014,\n title = {Neuroinflammation and β amyloid deposition in {Alzheimer}'s disease: in vivo quantification with molecular imaging},\n volume = {37},\n issn = {1421-9824},\n shorttitle = {Neuroinflammation and β amyloid deposition in {Alzheimer}'s disease},\n doi = {10.1159/000354363},\n abstract = {BACKGROUND/AIMS: Neuroinflammation plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Its relationship with underlying β amyloid deposition remains unclear. In vivo visualization of microglial activation has become possible with the development of molecular imaging ligands when used with positron emission tomography (PET). The translocator protein (TSPO) is upregulated during neuroinflammation. Consequently, targeting TSPO with radiolabeled ligands for PET is an attractive biomarker for neuroinflammation.\nMETHODS: A review of the research literature on PET imaging which studied in vivo neuroinflammation in AD subjects and its relationship with amyloid load was performed, including papers published between 2001 and 2012.\nRESULTS: Six studies were included using either [(11)C]PK-11195 or another non-TSPO radioligand that binds to the monoaminooxidase B. All the studies evaluated amyloid load with [(11)C]PIB. Microglial activation and astrocytosis are potentially early phenomena in AD. However, the individual levels of amyloid deposition and microglial activation were not correlated.\nCONCLUSION: Noninvasive in vivo molecular imaging to visualize neuroinflammation in AD may contribute to our understanding of the kinetics of neuroinflammation and its relationship to the hallmarks of the disease. Both are important for the development of future therapeutic modalities and for quantifying the efficacy of future disease-modifying treatments.},\n language = {eng},\n number = {1-2},\n journal = {Dementia and Geriatric Cognitive Disorders},\n author = {Hommet, C. and Mondon, K. and Camus, V. and Ribeiro, M. J. and Beaufils, E. and Arlicot, N. and Corcia, P. and Paccalin, M. and Minier, F. and Gosselin, T. and Page, G. and Guilloteau, D. and Chalon, S.},\n year = {2014},\n pmid = {24107621},\n keywords = {Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Benzothiazoles, Brain, Humans, Inflammation, Isoquinolines, Mitochondrial ADP, ATP Translocases, Molecular Imaging, Monoamine Oxidase, Positron-Emission Tomography, Radiopharmaceuticals, tau Proteins},\n pages = {1--18}\n}","bibtype":"article","doi":"10.1159/000354363","id":"hommet_neuroinflammation_2014","issn":"1421-9824","journal":"Dementia and Geriatric Cognitive Disorders","key":"hommet_neuroinflammation_2014","keywords":"Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Benzothiazoles, Brain, Humans, Inflammation, Isoquinolines, Mitochondrial ADP, ATP Translocases, Molecular Imaging, Monoamine Oxidase, Positron-Emission Tomography, Radiopharmaceuticals, tau Proteins","language":"eng","number":"1-2","pages":"1--18","pmid":"24107621","shorttitle":"Neuroinflammation and β amyloid deposition in Alzheimer's disease","title":"Neuroinflammation and β amyloid deposition in Alzheimer's disease: in vivo quantification with molecular imaging","type":"article","volume":"37","year":"2014","bibbaseid":"hommet-mondon-camus-ribeiro-beaufils-arlicot-corcia-paccalin-minier-gosselin-page-guilloteau-chalon-neuroinflammationandamyloiddepositioninalzheimersdiseaseinvivoquantificationwithmolecularimaging-2014","role":"author","urls":{},"keyword":["Aged","Aged","80 and over","Alzheimer Disease","Amyloid beta-Peptides","Benzothiazoles","Brain","Humans","Inflammation","Isoquinolines","Mitochondrial ADP","ATP Translocases","Molecular Imaging","Monoamine Oxidase","Positron-Emission Tomography","Radiopharmaceuticals","tau Proteins"],"downloads":0},"bibtype":"article","biburl":"https://api.zotero.org/users/1159944/collections/M6TABHZN/items?key=1pvuA2LY3hAaGNWuGNZF2QkP&format=bibtex&limit=100","creationDate":"2015-02-11T08:49:20.256Z","downloads":0,"keywords":["aged","aged","80 and over","alzheimer disease","amyloid beta-peptides","benzothiazoles","brain","humans","inflammation","isoquinolines","mitochondrial adp","atp translocases","molecular imaging","monoamine oxidase","positron-emission tomography","radiopharmaceuticals","tau proteins"],"search_terms":["neuroinflammation","amyloid","deposition","alzheimer","disease","vivo","quantification","molecular","imaging","hommet","mondon","camus","ribeiro","beaufils","arlicot","corcia","paccalin","minier","gosselin","page","guilloteau","chalon"],"title":"Neuroinflammation and β amyloid deposition in Alzheimer's disease: in vivo quantification with molecular imaging","year":2014,"dataSources":["Jekqva3EtgNgLZ4ic"]}