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The aged rhesus macaque manifests Braak stage III/IV Alzheimer's‐like pathology
Author(s) -
Paspalas Constantinos D.,
Carlyle Becky C.,
Leslie Shan,
Preuss Todd M.,
Crimins Johanna L.,
Huttner Anita J.,
Dyck Christopher H.,
Rosene Douglas L.,
Nairn Angus C.,
Arnsten Amy F.T.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.11.005
Subject(s) - entorhinal cortex , macaque , rhesus macaque , neuroscience , pathology , neuropathology , cortex (anatomy) , prefrontal cortex , neurodegeneration , alzheimer's disease , amyloid (mycology) , psychology , disease , hippocampus , biology , medicine , cognition , immunology
Abstract Introduction An animal model of late‐onset Alzheimer's disease is needed to research what causes degeneration in the absence of dominant genetic insults and why the association cortex is particularly vulnerable to degeneration. Methods We studied the progression of tau and amyloid cortical pathology in the aging rhesus macaque using immunoelectron microscopy and biochemical assays. Results Aging macaques exhibited the same qualitative pattern and sequence of tau and amyloid cortical pathology as humans, reaching Braak stage III/IV. Pathology began in the young‐adult entorhinal cortex with protein kinase A‐phosphorylation of tau, progressing to fibrillation with paired helical filaments and mature tangles in oldest animals. Tau pathology in the dorsolateral prefrontal cortex paralleled but lagged behind the entorhinal cortex, not afflicting the primary visual cortex. Discussion The aging rhesus macaque provides the long‐sought animal model for exploring the etiology of late‐onset Alzheimer's disease and for testing preventive strategies.