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Neurobiol Aging. 2017 Nov;59:107-120. doi: 10.1016/j.neurobiolaging.2017.07.006. Epub 2017 Aug 1.

Aged chimpanzees exhibit pathologic hallmarks of Alzheimer's disease.

Author information

1
School of Biomedical Sciences, Kent State University, Kent, OH, USA; Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA. Electronic address: medler@neomed.edu.
2
Department of Anthropology and Center for the Advanced Study of Human Paleobiology, The George Washington University, Washington, DC, USA.
3
Department of Anthropology, Kent State University, Kent, OH, USA.
4
Division of Developmental and Cognitive Neuroscience, Yerkes National Primate Research Center, Atlanta, GA, USA; Neuroscience Institute, Georgia State University, Atlanta, GA, USA.
5
MAEBIOS, Alamogordo, NM, USA.
6
Departments of Neurobiology and Neurology, Barrow Neurological Institute, Phoenix, AZ, USA.
7
Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; New York Consortium for Evolutionary Primatology, New York, NY, USA.
8
School of Biomedical Sciences, Kent State University, Kent, OH, USA; Department of Anthropology, Kent State University, Kent, OH, USA.

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.

KEYWORDS:

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

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