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Previous Volume 331:1091-1092 October 20, 1994 Number 16 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Few diseases are as debilitating and inevitably lethal as amyotrophic lateral sclerosis (ALS). The disease typically strikes adults in midlife, causing paralysis and death within five years. The cause of most cases remains unknown, and the disease is untreatable. About 10 percent of patients have an inherited form of the disease. In 1993 a multicenter study reported that some cases of familial ALS arise because of mutations in the gene encoding the cytosolic form of the enzyme copper-zinc superoxide dismutase (SOD1).¹ This enzyme detoxifies the superoxide anion, a ubiquitous byproduct of aerobic metabolism. As a free radical (free to diffuse . . . [Full Text of this Article]

References

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Transgenic-Mouse Model of Amyotrophic Lateral Sclerosis
Gurney M. E.
Extract | Full Text  
N Engl J Med 1994; 331:1721-1722, Dec 22, 1994. Correspondence

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• Yoshida, T., Maulik, N., Engelman, R. M., Ho, Y.-S., Das, D. K. (2000). Targeted Disruption of the Mouse Sod I Gene Makes the Hearts Vulnerable to Ischemic Reperfusion Injury. Circ. Res. 86: 264-269 [Abstract] [Full Text]  
• Gurney, M. E. (1994). Transgenic-Mouse Model of Amyotrophic Lateral Sclerosis. NEJM 331: 1721-1722 [Full Text]