Glutamatergic treatment strategies for age-related memory disorders

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Abstract

Age-related changes of N-methyl-D-aspartate (NMDA) receptors have been found in cortical areas and in the hippocampus of many species. On the basis of a variety of experimental observations it has been suggested that the decrease of NMDA receptor density might be one of the causative factors of the cognitive decline with aging. Based on these findings several strategies have been developed to improve cognition by compensating the NMDA receptor deficits in aging. The most promising approaches are the indirect activation of glutamatergic neurotransmission by agonists of the glycine site or the restoration of the age-related deficit of receptor density by several nootropics.

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      The NMDA and AMPA ionotropic glutamate receptor subtypes are critical for long-term potentiation and hippocampal-dependent learning and memory (Riedel et al., 2003). A reduction in ionotropic receptors and their constituent subunits with age has been correlated with a decline in memory function (Magnusson, 1998a,b; Adams et al., 2001; Tang et al., 2001; Clayton et al., 2002), which can be modulated with pharmacological agents that facilitate activation of the glutamate receptors (Müller et al., 1994; Wu et al., 2002; Rosenzweig and Barnes, 2003). Thus, age-related changes in presynaptic and glial regulation of glutamate release may be needed to help explain age-related changes in hippocampal neuron function during aging.

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