Does modulation of glutamatergic function represent a viable therapeutic strategy in Alzheimer's disease?
Although glutamate dysfunction has been implicated in the pathogenesis of Alzheimer's disease (AD), it is unclear which direction a glutamatergic strategy should take in this illness. Increasing glutamate function may enhance excitotoxicity and neuronal death, whereas decreasing activity in this excitatory amino acid pathway may impair memory processes. Pharmacological modulation of the different NMDA and nonNMDA receptor sites, together with the concept of an agonist versus antagonist approach, are discussed in this review. It would appear that a glutamatergic approach may represent a new and exciting option to pursue in the experimental pharmacotherapeutics of AD.
Department of Psychiatry, Mount Sinai School of Medicine, New York, NY.
B A
BA
Lawlor
K L
KL
Davis
D000368:Aged; D000544:Alzheimer Disease / Q000188:drug therapy* / Q000503:physiopathology / Q000523:psychology; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D005971:Glutamates / Q000502:physiology*; D018698:Glutamic Acid; D006801:Humans; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors* / Q000502:physiology; D017981:Receptors, Neurotransmitter / Q000037:antagonists & inhibitors* / Q000502:physiology
D005971:Glutamates; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D018698:Glutamic Acid