Accumulated evidence implies that mutations in the gene coding for Cu/Zn superoxide dismutase (SOD) are associated with the pathogenesis of the familial form of amyotrophic lateral sclerosis (ALS). The clinical and pathological similarities of the familial and the sporadic forms of the disease may suggest that abnormal SOD activity takes also part in the pathogenesis of sporadic ALS. We therefore measured serum SOD activity in fifteen sporadic ALS patients. Mean serum SOD activity was 1.15 ± 0.40 u/ml in ALS patients, 1.50 ± 0.45 u/ml in patients with other neurological disorders and 1.45 ± 0.45 u/ml in healthy controls (p < 0.021 and p < 0.031 respectively). If this sporadic ALS-related reduction in serum SOD activity will be confirmed in the diseased nervous system tissue; it may suggest that abnormal SOD activity is also associated with the motor neuron damage in the sporadic form of ALS.
Bibliographical noteFunding Information:
This research was supported in part by the Fanni Rubin Steinpress Research Endowment Fund and in part by the Hilda Katz Blaustein Fund and the Nina Silverman Memorial Neurological Endowment Fund.
- Amyotrophic lateral sclerosis
- Free radical
- Superoxide dismutase