Aged chimpanzees exhibit pathologic hallmarks of Alzheimer's disease.

Aged chimpanzees exhibit pathologic hallmarks of Alzheimer's disease.

Edler Melissa K; Sherwood Chet C; Meindl Richard S; Hopkins William D; Ely John J; Erwin Joseph M; Mufson Elliott J; Hof Patrick R; Raghanti Mary Ann

Neurobiology of aging

2017

2017-11

Alzheimer's disease (AD) is a uniquely human brain disorder characterized by the accumulation of amyloid-beta protein (Abeta) 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 Abeta and tau lesions in brain regions affected by AD in humans. Abeta was observed in plaques and blood vessels, and tau lesions were found in the form of pretangles, NFT, and tau-immunoreactive neuritic clusters. Abeta 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 Abeta 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.

*Alzheimer's disease; *Amyloid-beta protein; *Chimpanzee; *Neurofibrillary tangle; *Primate; *Tau; Aging/*metabolism/*pathology; Alzheimer Disease/*metabolism/*pathology; Amyloid beta-Peptides/metabolism; Animals; Brain/*metabolism/*pathology; Female; Humans; Male; Neurofibrillary Tangles/metabolism/pathology; Pan troglodytes; tau Proteins/metabolism

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