Rates of ,B-amyloid deposition indicate widespread simultaneous accumulation throughout the brain

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.

Automated summary

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.