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Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis

Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis Recently, the excitatory amino acid neurotransmitter glutamate was implicated in the pathogenesis of a variety of chronic degenerative neurological diseases in humans and animals. This report describes abnormalities in excitatory amino acids in the central nervous system of 18 patients with amyotrophic lateral sclerosis (ALS). The concentration of the excitatory amino acids glutamate and aspartate in the cerebrospinal fluid were increased significantly (p > 0.01) by 100 to 200% in patients with ALS. Similarly, the concentrations of the excitatory neuropeptide N‐acetyl‐aspartyl glutamate and its metabolite, N‐acetyl‐aspartate, were elevated twofold to threefold in the cerebrospinal fluid from the patients. There was no relationship between amino acid concentrations and duration of disease, clinical impairment, or patient age. In the ventral horns of the cervical region of the spinal cord, the level of N‐acetyl‐‐aspartyl glutamate and N‐acetyl‐aspartate was decreased by 60% (p > 0.05) and 40% (p > 0.05), respectively, in 8 patients with ALS. Choline acetyltransferase activity was also diminished by 35% in the ventral horn consistent with motor neuron loss. We conclude that excitatory amino acid metabolism is altered in patients with ALS. Based on neurodegenerative disease models, these changes may play a role in motor neuron loss in ALS. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis

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References (69)

Publisher
Wiley
Copyright
Copyright © 1990 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.410280106
pmid
2375630
Publisher site
See Article on Publisher Site

Abstract

Recently, the excitatory amino acid neurotransmitter glutamate was implicated in the pathogenesis of a variety of chronic degenerative neurological diseases in humans and animals. This report describes abnormalities in excitatory amino acids in the central nervous system of 18 patients with amyotrophic lateral sclerosis (ALS). The concentration of the excitatory amino acids glutamate and aspartate in the cerebrospinal fluid were increased significantly (p > 0.01) by 100 to 200% in patients with ALS. Similarly, the concentrations of the excitatory neuropeptide N‐acetyl‐aspartyl glutamate and its metabolite, N‐acetyl‐aspartate, were elevated twofold to threefold in the cerebrospinal fluid from the patients. There was no relationship between amino acid concentrations and duration of disease, clinical impairment, or patient age. In the ventral horns of the cervical region of the spinal cord, the level of N‐acetyl‐‐aspartyl glutamate and N‐acetyl‐aspartate was decreased by 60% (p > 0.05) and 40% (p > 0.05), respectively, in 8 patients with ALS. Choline acetyltransferase activity was also diminished by 35% in the ventral horn consistent with motor neuron loss. We conclude that excitatory amino acid metabolism is altered in patients with ALS. Based on neurodegenerative disease models, these changes may play a role in motor neuron loss in ALS.

Journal

Annals of Neurology – Wiley

Published: Jul 1, 1990

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