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Tracy Hampton, PhD

JAMA. 2007;298(17):1998.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Deleting a single gene nearly doubles the lifespan of mice with the neurodegenerative disease amyotrophic lateral sclerosis (ALS), report scientists at the University of Iowa, in Iowa City (Marden JJ et al. J Clin Invest. 2007;117[10]:2913-2919). The findings suggest that the gene may be a target for therapies in humans.

Animal research has shown that chemically reactive forms of oxygen that can damage cells contributes to the development of ALS. In this recent study, investigators studied two proteins present in mice and humans that are known to generate reactive oxygen species. They found that getting rid of one of these, Nox2, slowed the progression of ALS and improved survival in mice with the disease.

The team found that ALS mice lacking the gene that encodes Nox2 produced fewer reactive oxygen species and lived on average for 229 days, 97 days longer than those with normal levels . . . [Full Text of this Article]