Lookup NU author(s): Dr Mark Cookson,
Professor Pamela Shaw
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Several studies have suggested that excessive generation of nitric oxide (NO) may contribute to the pathogenesis of amyotrophic lateral sclerosis (ALS). Recently, a selective induction of the neuronal isoform of nitric oxide synthase (nNOS) in glial cells has been reported in an animal model of familial ALS. We therefore examined in postmortem tissue the expression of nNOS in patients with sporadic ALS and patients without any history of neurological disease. Using immunohistochemistry, we found an up-regulation of nNOS in glial cells of the spinal cord and subcortical white matter in ALS patients compared to controls. The enhanced glial nNOS expression seen in ALS patients could conceivably contribute to motoneuronal degeneration through NO-mediated cytotoxic effects. © 2001 Academic Press.
Author(s): Anneser JMH, Cookson MR, Ince PG, Shaw PJ, Borasio GD
Publication type: Article
Publication status: Published
Journal: Experimental Neurology
ISSN (print): 0014-4886
ISSN (electronic): 1090-2430
Publisher: Academic Press
PubMed id: 11573993
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