Journal
NEUROBIOLOGY OF AGING
Volume 115, Issue -, Pages 1-11Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2022.03.005
Keywords
Aging; Amyloid; Tau; APOE; Alzheimer's Disease; Longitudinal
Categories
Funding
- National Institutes of Health [AG034570, AG062542]
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This study used PIB-PET imaging to investigate the progression of regional amyloid accumulation in cognitively normal older adults, finding that amyloid accumulates near-simultaneously throughout the brain and is associated with higher AD pathology. Carriers of the apolipoprotein-E e 4 allele had faster amyloid accumulation, and faster accumulation was associated with greater tau burden in most brain regions.
Amyloid plaque aggregation is a pathologic hallmark of Alzheimer's disease (AD) that occurs early in the disease. However, little is known about its progression throughout the brain. Using Pittsburgh Compound B (PIB)-PET imaging, we investigated the progression of regional amyloid accumulation in cognitively normal older adults. We found that all examined regions reached their peak accumulation rates 24-28 years after an estimated initiation corresponding to the mean baseline PIB-PET signal in amyloid-negative older adults. We also investigated the effect of increased genetic risk conferred by the apolipoprotein-E e 4 allele on rates of amyloid accumulation, as well as the relationship between regional amyloid accu-mulation and regional tau pathology, another hallmark of AD, measured with Flortaucipir-PET. Carriers of the e 4 allele had faster amyloid accumulation in all brain regions. Furthermore, in all regions excluding the temporal lobe, faster amyloid accumulation was associated with greater tau burden. These results in-dicate that amyloid accumulates near-simultaneously throughout the brain and is associated with higher AD pathology, and that genetic risk of AD is associated with faster amyloid accumulation.(c) 2022 Elsevier Inc. All rights reserved.
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