Abstract

Aged nonhuman primates develop many of the neurobiological hallmarks of aging that occur in humans, including degenerative and compensatory neuronal changes, senile plaques, and cerebrovascular β-amyloidosis. Alterations in neurons and their transmitters are often subtle and variable in monkeys, making correlations between cerebral and behavioral changes difficult to detect and interpret. Future studies should increasingly focus on specific phenomena that are characteristic of the senescent primate brain. For example, monkeys presently are the best animal model of cerebral βamyloidosis, and have yielded significant data on the composition of senile plaques. With the development of new methods for studying β-amyloid in primates, we can achieve important new insights into the genesis, detection and treatment of age-associated diseases such as cerebrovascular amyloidosis and Alzheimer's disease.

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