4.3 Review

Comparative neuropathology in aging primates: A perspective

Journal

AMERICAN JOURNAL OF PRIMATOLOGY
Volume 83, Issue 11, Pages -

Publisher

WILEY
DOI: 10.1002/ajp.23299

Keywords

brain senescence; glia; neuron morphology; non-human primates; proteinopathy

Categories

Funding

  1. National Institutes of Health [AG005138, AG014308, AG014449, AG046266, AG049870, AG059028, AG066514, AG067419]

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Research indicates that non-human primates exhibit more variable expressions of pathological alterations among individuals and species, providing an opportunity to study brain aging. Age-related changes at neuronal population, single cell, and synaptic levels have been well documented in macaques and marmosets, while additional species including lemurs and great apes also show age-related and Alzheimer's disease-like neuropathology.
While humans exhibit a significant degree of neuropathological changes associated with deficits in cognitive and memory functions during aging, non-human primates (NHP) present with more variable expressions of pathological alterations among individuals and species. As such, NHP with long life expectancy in captivity offer an opportunity to study brain senescence in the absence of the typical cellular pathology caused by age-related neurodegenerative illnesses commonly seen in humans. Age-related changes at neuronal population, single cell, and synaptic levels have been well documented in macaques and marmosets, while age-related and Alzheimer's disease-like neuropathology has been characterized in additional species including lemurs as well as great apes. We present a comparative overview of existing neuropathologic observations across the primate order, including classic age-related changes such as cell loss, amyloid deposition, amyloid angiopathy, and tau accumulation. We also review existing cellular and ultrastructural data on neuronal changes, such as dendritic attrition and spine alterations, synaptic loss and pathology, and axonal and myelin pathology, and discuss their repercussions on cellular and systems function and cognition.

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