Abstract
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].
Highlights
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
Reduced NMDA expression is associated with aging in macaque monkeys and rats [3]
Combining single cell and network modeling methods, we investigated the hypothesis that decreased synaptic NMDA conductance is sufficient to cause network-level deficits in "discrete-attractor" working-memory tasks.These tasks can be modeled with a network of recurrently connected model neurons in which the synapses are tuned according to a Hebbian pattern, so that synaptic reverberation enables the network to store and respond to specific input patterns [4]
Summary
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. Address: 1Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA, 2Laboratory of Biomathematics, Mount Sinai School of Medicine, New York, NY 10029, USA, 3Computational Neurobiology and Imaging Center, Mount Sinai School of Medicine, New York, NY 10029, USA and 4Dept of Psychiatry, Boston University, Boston, MA 02118, USA Email: Patrick J Coskren* - pcoskren@mac.com * Corresponding author from Seventeenth Annual Computational Neuroscience Meeting: CNS*2008 Portland, OR, USA.
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