Prevalence of amyloid PET positivity in dementia syndromes: a meta-analysis. Ossenkoppele, R., Jansen, W. J., Rabinovici, G. D., Knol, D. L., van der Flier, W. M., van Berckel, B. N. M., Scheltens, P., Visser, P. J., Amyloid PET Study Group, Verfaillie, S. C. J., Zwan, M. D., Adriaanse, S. M., Lammertsma, A. A., Barkhof, F., Jagust, W. J., Miller, B. L., Rosen, H. J., Landau, S. M., Villemagne, V. L., Rowe, C. C., Lee, D. Y., Na, D. L., Seo, S. W., Sarazin, M., Roe, C. M., Sabri, O., Barthel, H., Koglin, N., Hodges, J., Leyton, C. E., Vandenberghe, R., van Laere, K., Drzezga, A., Forster, S., Grimmer, T., Sánchez-Juan, P., Carril, J. M., Mok, V., Camus, V., Klunk, W. E., Cohen, A. D., Meyer, P. T., Hellwig, S., Newberg, A., Frederiksen, K. S., Fleisher, A. S., Mintun, M. A., Wolk, D. A., Nordberg, A., Rinne, J. O., Chételat, G., Lleo, A., Blesa, R., Fortea, J., Madsen, K., Rodrigue, K. M., & Brooks, D. J. JAMA, 313(19):1939--1949, May, 2015.
doi  abstract   bibtex   
IMPORTANCE: Amyloid-β positron emission tomography (PET) imaging allows in vivo detection of fibrillar plaques, a core neuropathological feature of Alzheimer disease (AD). Its diagnostic utility is still unclear because amyloid plaques also occur in patients with non-AD dementia. OBJECTIVE: To use individual participant data meta-analysis to estimate the prevalence of amyloid positivity on PET in a wide variety of dementia syndromes. DATA SOURCES: The MEDLINE and Web of Science databases were searched from January 2004 to April 2015 for amyloid PET studies. STUDY SELECTION: Case reports and studies on neurological or psychiatric diseases other than dementia were excluded. Corresponding authors of eligible cohorts were invited to provide individual participant data. DATA EXTRACTION AND SYNTHESIS: Data were provided for 1359 participants with clinically diagnosed AD and 538 participants with non-AD dementia. The reference groups were 1849 healthy control participants (based on amyloid PET) and an independent sample of 1369 AD participants (based on autopsy). MAIN OUTCOMES AND MEASURES: Estimated prevalence of positive amyloid PET scans according to diagnosis, age, and apolipoprotein E (APOE) ε4 status, using the generalized estimating equations method. RESULTS: The likelihood of amyloid positivity was associated with age and APOE ε4 status. In AD dementia, the prevalence of amyloid positivity decreased from age 50 to 90 years in APOE ε4 noncarriers (86% [95% CI, 73%-94%] at 50 years to 68% [95% CI, 57%-77%] at 90 years; n = 377) and to a lesser degree in APOE ε4 carriers (97% [95% CI, 92%-99%] at 50 years to 90% [95% CI, 83%-94%] at 90 years; n = 593; P \textless .01). Similar associations of age and APOE ε4 with amyloid positivity were observed in participants with AD dementia at autopsy. In most non-AD dementias, amyloid positivity increased with both age (from 60 to 80 years) and APOE ε4 carriership (dementia with Lewy bodies: carriers [n = 16], 63% [95% CI, 48%-80%] at 60 years to 83% [95% CI, 67%-92%] at 80 years; noncarriers [n = 18], 29% [95% CI, 15%-50%] at 60 years to 54% [95% CI, 30%-77%] at 80 years; frontotemporal dementia: carriers [n = 48], 19% [95% CI, 12%-28%] at 60 years to 43% [95% CI, 35%-50%] at 80 years; noncarriers [n = 160], 5% [95% CI, 3%-8%] at 60 years to 14% [95% CI, 11%-18%] at 80 years; vascular dementia: carriers [n = 30], 25% [95% CI, 9%-52%] at 60 years to 64% [95% CI, 49%-77%] at 80 years; noncarriers [n = 77], 7% [95% CI, 3%-18%] at 60 years to 29% [95% CI, 17%-43%] at 80 years. CONCLUSIONS AND RELEVANCE: Among participants with dementia, the prevalence of amyloid positivity was associated with clinical diagnosis, age, and APOE genotype. These findings indicate the potential clinical utility of amyloid imaging for differential diagnosis in early-onset dementia and to support the clinical diagnosis of participants with AD dementia and noncarrier APOE ε4 status who are older than 70 years.
@article{ossenkoppele_prevalence_2015,
	title = {Prevalence of amyloid {PET} positivity in dementia syndromes: a meta-analysis},
	volume = {313},
	issn = {1538-3598},
	shorttitle = {Prevalence of amyloid {PET} positivity in dementia syndromes},
	doi = {10.1001/jama.2015.4669},
	abstract = {IMPORTANCE: Amyloid-β positron emission tomography (PET) imaging allows in vivo detection of fibrillar plaques, a core neuropathological feature of Alzheimer disease (AD). Its diagnostic utility is still unclear because amyloid plaques also occur in patients with non-AD dementia.
OBJECTIVE: To use individual participant data meta-analysis to estimate the prevalence of amyloid positivity on PET in a wide variety of dementia syndromes.
DATA SOURCES: The MEDLINE and Web of Science databases were searched from January 2004 to April 2015 for amyloid PET studies.
STUDY SELECTION: Case reports and studies on neurological or psychiatric diseases other than dementia were excluded. Corresponding authors of eligible cohorts were invited to provide individual participant data.
DATA EXTRACTION AND SYNTHESIS: Data were provided for 1359 participants with clinically diagnosed AD and 538 participants with non-AD dementia. The reference groups were 1849 healthy control participants (based on amyloid PET) and an independent sample of 1369 AD participants (based on autopsy).
MAIN OUTCOMES AND MEASURES: Estimated prevalence of positive amyloid PET scans according to diagnosis, age, and apolipoprotein E (APOE) ε4 status, using the generalized estimating equations method.
RESULTS: The likelihood of amyloid positivity was associated with age and APOE ε4 status. In AD dementia, the prevalence of amyloid positivity decreased from age 50 to 90 years in APOE ε4 noncarriers (86\% [95\% CI, 73\%-94\%] at 50 years to 68\% [95\% CI, 57\%-77\%] at 90 years; n = 377) and to a lesser degree in APOE ε4 carriers (97\% [95\% CI, 92\%-99\%] at 50 years to 90\% [95\% CI, 83\%-94\%] at 90 years; n = 593; P {\textless} .01). Similar associations of age and APOE ε4 with amyloid positivity were observed in participants with AD dementia at autopsy. In most non-AD dementias, amyloid positivity increased with both age (from 60 to 80 years) and APOE ε4 carriership (dementia with Lewy bodies: carriers [n = 16], 63\% [95\% CI, 48\%-80\%] at 60 years to 83\% [95\% CI, 67\%-92\%] at 80 years; noncarriers [n = 18], 29\% [95\% CI, 15\%-50\%] at 60 years to 54\% [95\% CI, 30\%-77\%] at 80 years; frontotemporal dementia: carriers [n = 48], 19\% [95\% CI, 12\%-28\%] at 60 years to 43\% [95\% CI, 35\%-50\%] at 80 years; noncarriers [n = 160], 5\% [95\% CI, 3\%-8\%] at 60 years to 14\% [95\% CI, 11\%-18\%] at 80 years; vascular dementia: carriers [n = 30], 25\% [95\% CI, 9\%-52\%] at 60 years to 64\% [95\% CI, 49\%-77\%] at 80 years; noncarriers [n = 77], 7\% [95\% CI, 3\%-18\%] at 60 years to 29\% [95\% CI, 17\%-43\%] at 80 years.
CONCLUSIONS AND RELEVANCE: Among participants with dementia, the prevalence of amyloid positivity was associated with clinical diagnosis, age, and APOE genotype. These findings indicate the potential clinical utility of amyloid imaging for differential diagnosis in early-onset dementia and to support the clinical diagnosis of participants with AD dementia and noncarrier APOE ε4 status who are older than 70 years.},
	language = {eng},
	number = {19},
	journal = {JAMA},
	author = {Ossenkoppele, Rik and Jansen, Willemijn J. and Rabinovici, Gil D. and Knol, Dirk L. and van der Flier, Wiesje M. and van Berckel, Bart N. M. and Scheltens, Philip and Visser, Pieter Jelle and {Amyloid PET Study Group} and Verfaillie, Sander C. J. and Zwan, Marissa D. and Adriaanse, Sofie M. and Lammertsma, Adriaan A. and Barkhof, Frederik and Jagust, William J. and Miller, Bruce L. and Rosen, Howard J. and Landau, Susan M. and Villemagne, Victor L. and Rowe, Christopher C. and Lee, Dong Y. and Na, Duk L. and Seo, Sang W. and Sarazin, Marie and Roe, Catherine M. and Sabri, Osama and Barthel, Henryk and Koglin, Norman and Hodges, John and Leyton, Cristian E. and Vandenberghe, Rik and van Laere, Koen and Drzezga, Alexander and Forster, Stefan and Grimmer, Timo and Sánchez-Juan, Pascual and Carril, Jose M. and Mok, Vincent and Camus, Vincent and Klunk, William E. and Cohen, Ann D. and Meyer, Philipp T. and Hellwig, Sabine and Newberg, Andrew and Frederiksen, Kristian S. and Fleisher, Adam S. and Mintun, Mark A. and Wolk, David A. and Nordberg, Agneta and Rinne, Juha O. and Chételat, Gaël and Lleo, Alberto and Blesa, Rafael and Fortea, Juan and Madsen, Karine and Rodrigue, Karen M. and Brooks, David J.},
	month = may,
	year = {2015},
	pmid = {25988463},
	pages = {1939--1949}
}
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