α2-adrenergic mechanisms in prefrontal cortex associated with cognitive decline in aged nonhuman primates

Abstract

This study provides evidence that the α2-adrenergic receptor agonist clonidine ameliorates the cognitive deficits exhibited by aged nonhuman primates through drug actions at 0.2 receptors. Furthermore, pharmacological profiles in animals with lesions restricted to the dorsolateral prefrontal cortex indicate that this area may be the site of action for some of clonidine's beneficial effects. These results demonstrate that α-adrenergic systems contribute to cognitive function and suggest a new strategy for treating memory disorders in aged humans.