| NEUROBIOLOGY OF AGING | 卷:36 |
| Commentary: is Alzheimer's disease uniquely human? | |
| Article | |
| Finch, Caleb E.1,2  Austad, Steven N.3  | |
| [1] Univ So Calif, Davis Sch Gerontol, Los Angeles, CA 90089 USA | |
| [2] Univ So Calif, Dept Biol Sci, Los Angeles, CA 90089 USA | |
| [3] Univ Alabama Birmingham, Dept Biol, Birmingham, AL 35294 USA | |
| 关键词: Alzheimer's disease; Aging; Chimpanzee; Gorilla; Obesity; Life span; | |
| DOI : 10.1016/j.neurobiolaging.2014.10.025 | |
| 来源: Elsevier | |
PDF
|
|
【 摘 要 】
That Alzheimer's disease (AD) might be a human-specific disease was hypothesized by Rapoport in 1989. Apes and humans share an identical amyloid beta (A beta) peptide amino acid sequence and accumulate considerable A beta deposits after age 40 years, an age when amyloid plaques are uncommon in humans. Despite their early A beta buildup, ape brains have not shown evidence dystrophic neurites near plaques. Aging great ape brains also have few neurofibrillary tangles, with one exception of 1 obese chimpanzee euthanized after a stroke who displayed abundant neurofibrillary tangles, but without the typical AD distribution. We discuss the need for more exacting evaluation of neuron density with age, and note husbandry issues that may allow great apes to live to greater ages. We remain reserved about expectations for fully developed AD-like pathology in the great apes of advanced ages and cautiously support Rapoport's hypothesis. (C) 2015 Elsevier Inc. All rights reserved.
【 授权许可】
Free
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| 10_1016_j_neurobiolaging_2014_10_025.pdf | 249KB |
PDF