Excitotoxicity and Neurodegeneration

The discovery of the excitotoxic effects of glutamate fuelled speculation that a similar mechanism might underlie neuronal cell death in chronic neurode-generative diseases such as Alzheimer's disease, Huntingdon's disease and amyotrophic lateral sclerosis (ALS). Several studies have examined whether the subunit composition of AMPARs is altered in these states to produce GluR with higher Ca2+ permeability. A reduction in GluR2 expression has been observed in spinal motor neurones in ALS patients, which would be consistent with an enhanced Ca2+ permeability and excitotoxicity (Virgo et al., 1996). The level of GluR2 expression is also decreased in pyramidal neurones of the parahippocampal gyrus in patients with schizophrenia (Eastwood et al., 1995). Whether these changes in GluR2 levels are the principal cause, or simply a consequence, of these disease, however, remains unknown.

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