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Ann Neurol. 1990 Jul;28(1):3-8.

Glutamate dysfunction and selective motor neuron degeneration in amyotrophic lateral sclerosis: a hypothesis.

Author information

1
Mount Sinai School of Medicine, New York, NY 10029.

Abstract

Recent studies provided evidence for a generalized defect in glutamate metabolism in patients with amyotrophic lateral sclerosis, associated with widespread alterations in the central nervous system levels of this excitatory amino acid putative transmitter. Present data support the hypothesis that altered presynaptic glutamatergic mechanisms may be responsible for a neuroexcitotoxic cell loss in this disorder. High local concentrations of glycine, released from glycinergic terminals, may disrupt adaptive processes contributing to abnormal potentiation of excitatory transmission mediated by glutamate receptors and resultant selective degeneration of motor neurons. These considerations offer new therapeutic strategies for amyotrophic lateral sclerosis.

PMID:
1973889
DOI:
10.1002/ana.410280103
[Indexed for MEDLINE]

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