toward understanding how genetics may influence the most common form of ALS,' said co-researcher Jeffrey D. Rothstein, professor in the Department of Neurology. 'The results will not only help us to better understand sporadic ALS but also to tailor tools that will reveal therapies for it.'

Traynor cautioned that the 34 SNPs are not guaranteed trail markers for ALS genes. 'If you roll dice 555,352 times, you are bound to get lucky by chance alone on some of those throws,' he said. 'The next step is to go back and figure out which of these 'hits' are real and which are false.' Thousands of other SNPs were more weakly associated with ALS, some of which could turn out to be just as important as those more strongly linked.

Traynor says a follow-up study is in the works that will replicate the research using a similar number of patients and controls. Traynor, who has a joint affiliation with the National Institute of Mental Health, collaborated in this study with lead author Jennifer Schymick and fellow researcher John Hardy, both of the Laboratory of Neurogenetics at the National Institute on Aging. Researchers from the National Institutes of Health, the Packard Center for ALS Research at Johns Hopkins and the University of Turin, Italy, also contributed to this study.

This study was supported by funding from the National Institute of Neurological Disorders and Stroke, the Packard Center for ALS Research at Johns Hopkins and the ALS Association.

Source-Eureka Alert
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