Abstract:
:Alzheimer's disease (AD) is a uniquely human brain disorder characterized by the accumulation of amyloid-beta protein (Aβ) 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 Aβ and tau lesions in brain regions affected by AD in humans. Aβ was observed in plaques and blood vessels, and tau lesions were found in the form of pretangles, NFT, and tau-immunoreactive neuritic clusters. Aβ 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 Aβ 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.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Edler MK,Sherwood CC,Meindl RS,Hopkins WD,Ely JJ,Erwin JM,Mufson EJ,Hof PR,Raghanti MAdoi
10.1016/j.neurobiolaging.2017.07.006subject
Has Abstractpub_date
2017-11-01 00:00:00pages
107-120eissn
0197-4580issn
1558-1497pii
S0197-4580(17)30239-7journal_volume
59pub_type
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