4.5 Article

Aged chimpanzees exhibit pathologic hallmarks of Alzheimer's disease

期刊

NEUROBIOLOGY OF AGING
卷 59, 期 -, 页码 107-120

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2017.07.006

关键词

Alzheimer's disease; Amyloid-beta protein; Chimpanzee; Neurofibrillary tangle; Primate; Tau

资金

  1. NSF [BCS-1316829]
  2. NIH [NS042867, NS073134, NS092988, AG017802, AG014308, AG005138, AG014449, AG043775]
  3. James S. McDonnell Foundation [220020293]
  4. Sigma Xi
  5. Kent State University Research Council
  6. Kent State University Graduate Student Senate
  7. Direct For Social, Behav & Economic Scie
  8. Division Of Behavioral and Cognitive Sci [1316829] Funding Source: National Science Foundation

向作者/读者索取更多资源

Alzheimer's disease (AD) is a uniquely human brain disorder characterized by the accumulation of amyloid-beta protein (Ab) into extracellular plaques, neurofibrillary tangles (NFT) made from intracellular, abnormally phosphorylated tau, and selective neuronal loss. We analyzed a large group of aged chimpanzees (n = 20, age 37-62 years) for evidence of Ab and tau lesions in brain regions affected by AD in humans. A beta was observed in plaques and blood vessels, and tau lesions were found in the form of pretangles, NFT, and tau-immunoreactive neuritic clusters. Ab deposition was higher in vessels than in plaques and correlated with increases in tau lesions, suggesting that amyloid build-up in the brain's microvasculature precedes plaque formation in chimpanzees. Age was correlated to greater volumes of Ab plaques and vessels. Tangle pathology was observed in individuals that exhibited plaques and moderate or severe cerebral amyloid angiopathy, a condition in which amyloid accumulates in the brain's vasculature. Amyloid and tau pathology in aged chimpanzees suggests these AD lesions are not specific to the human brain. (C) 2017 Elsevier Inc. All rights reserved.

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