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Specific cognitive deficits in working memory tasks are associated with normal aging in humans and nonhuman primates, even in the absence of pathologies such as Alzheimer's disease. Because normal aging does not involve widespread neuron death or gross morphological degeneration, the cause of these deficits remains unclear, although subtle anatomical and physiological effects are likely to play a causal role [1]. NMDA glutamate receptors in spines mediate synaptic communication and are critical in long-term potentiation (LTP) and learning. NMDA's dependence on postsynaptic depolarization has been proposed to enhance network stability through synaptic bistability [2]. Reduced NMDA expression is associated with aging in macaque monkeys and rats [3].

Network effects of age-related NMDA reduction in a model of working memory