TY - JOUR
T1 - β-amyloid burden in healthy aging
T2 - Regional distribution and cognitive consequences
AU - Rodrigue, K. M.
AU - Kennedy, K. M.
AU - Devous, M. D.
AU - Rieck, J. R.
AU - Hebrank, A. C.
AU - Diaz-Arrastia, R.
AU - Mathews, D.
AU - Park, D. C.
N1 - Funding Information:
Dr. Rodrigue receives research support from the NIH/NIA. Dr. Kennedy receives research support from the NIH/NIA. Dr. Devous served as an Associate Editor for Journal of Experimental Biology ; serves on a scientific advisory board for Avid Radiopharmaceuticals, Inc.; serves as a consultant for Avid Radiopharmaceuticals, Inc. and Bayer Schering Pharma; receives research support from Avid Radiopharmaceuticals, Inc., the NIH (NIA, NIDRR, NIDA), the US Department of Education, and the Alzheimer's Association; and holds stock in Avid Radiopharmaceuticals, Inc. A.C. Hebrank and J.R. Rieck report no disclosures. Dr. Diaz-Arrastia serves on the editorial board of the Journal of Neurotrauma and receives research support from the NIH/NIDRR and the Alzheimer's Association. Dr. Mathews reports no disclosures. Dr. Park receives research support from Avid Radiopharmaceuticals, Inc., the NIH/NIA, and the Alzheimer's Association; and her son litigated on behalf of Pfizer Inc.
Funding Information:
Supported by NIH grants 5R37AG-006265-25, 3R37AG-006265-25S1, and P30 AG12300 , and Alzheimer's Association grant IIRG-09-135087 . K.M.R. was supported in part by NIA grant 1K99-AG-036848-1 . The radiotracer was provided to the study by Avid Radiopharmaceuticals. The authors thank Michael Viguet for assistance with PET scanning, Chris Paliotta for collecting blood samples, and Gérard N. Bischof, Prasanna Tamil, and Erin Wooden for participant testing and scheduling.
PY - 2012/2/7
Y1 - 2012/2/7
N2 - Objective: Several lines of evidence suggest that pathologic changes underlying Alzheimer disease (AD) begin years prior to the clinical expression of the disease, underscoring the need for studies of cognitively healthy adults to capture these early changes. The overall goal of the current study was to map the cortical distribution of β-amyloid (Aβ) in a healthy adult lifespan sample (aged 30-89), and to assess the relationship between elevated amyloid and cognitive performance across multiple domains. Methods: A total of 137 well-screened and cognitively normal adults underwent Aβ PET imaging with radiotracer 18F-florbetapir. Aβ load was estimated from 8 cortical regions. Participants were genotyped for APOE and tested for processing speed, working memory, fluid reasoning, episodic memory, and verbal ability. Results: Aβ deposition is distributed differentially across the cortex and progresses at varying rates with age across cortical brain regions. A subset of cognitively normal adults aged 60 and over show markedly elevated deposition, and also had a higher rate of APOE ε4 (38%) than nonelevated adults (19%). Aβ burden was linked to poorer cognitive performance on measures of processing speed, working memory, and reasoning. Conclusions: Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status. Greater amyloid burden was related to deleterious effects on cognition, suggesting that subtle cognitive changes accrue as amyloid progresses.
AB - Objective: Several lines of evidence suggest that pathologic changes underlying Alzheimer disease (AD) begin years prior to the clinical expression of the disease, underscoring the need for studies of cognitively healthy adults to capture these early changes. The overall goal of the current study was to map the cortical distribution of β-amyloid (Aβ) in a healthy adult lifespan sample (aged 30-89), and to assess the relationship between elevated amyloid and cognitive performance across multiple domains. Methods: A total of 137 well-screened and cognitively normal adults underwent Aβ PET imaging with radiotracer 18F-florbetapir. Aβ load was estimated from 8 cortical regions. Participants were genotyped for APOE and tested for processing speed, working memory, fluid reasoning, episodic memory, and verbal ability. Results: Aβ deposition is distributed differentially across the cortex and progresses at varying rates with age across cortical brain regions. A subset of cognitively normal adults aged 60 and over show markedly elevated deposition, and also had a higher rate of APOE ε4 (38%) than nonelevated adults (19%). Aβ burden was linked to poorer cognitive performance on measures of processing speed, working memory, and reasoning. Conclusions: Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status. Greater amyloid burden was related to deleterious effects on cognition, suggesting that subtle cognitive changes accrue as amyloid progresses.
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U2 - 10.1212/WNL.0b013e318245d295
DO - 10.1212/WNL.0b013e318245d295
M3 - Article
C2 - 22302550
AN - SCOPUS:84858121162
SN - 0028-3878
VL - 78
SP - 387
EP - 395
JO - Neurology
JF - Neurology
IS - 6
ER -