Article: article from journal or magazin.
Glial cells of the spinal cord and subcortical white matter up-regulate neuronal nitric oxide synthase in sporadic amyotrophic lateral sclerosis.
Publication types: Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
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.
Aged, Cause of Death, Disease Models, Animal, Gene Expression Regulation, Enzymologic, Glial Fibrillary Acidic Protein/analysis, Glial Fibrillary Acidic Protein/genetics, Humans, Middle Aged, Motor Neuron Disease/enzymology, Motor Neuron Disease/pathology, Neuroglia/pathology, Neurons/enzymology, Neurons/pathology, Nitric Oxide Synthase/analysis, Nitric Oxide Synthase/genetics, Nitric Oxide Synthase Type I, Postmortem Changes, Spinal Cord/pathology
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