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Abstract
Point mutations in the cytosolic Cu/Zn superoxide dismutase (SOD-1) gene have been
detected in association with familial amyotrophic lateral sclerosis (FALS). SOD clears
superoxide radical and is one of the body's principal defense mechanisms against oxygen
toxicity. The finding of SOD variants in FALS is consistent with the hypothesis that
free radicals contribute to the pathogenesis of FALS, and possibly to the pathogenesis
of other neurodegenerative disorders such as Parkinson's disease, in which there is
substantial evidence of oxidant stress. The implication of free radicals in the pathogenesis
of neurodegenerative disorders raises the possibility that antioxidants might provide
neuroprotective therapy.