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Packard Center for ALS Research at Johns Hopkins

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Causes of ALS: Oxidative Damage

Studies of cells in certain ALS animal models and also in ALS patients have shown an increase in nervous system damage (oxidative damage) from free radicals. Apparently, the more the disease progresses, the greater the oxidative damage.

This idea is the basis for the anti-oxidant therapies that some patients currently take – anti-oxidant vitamins and medications meant to reverse this effect.

Free radicals are a common byproduct of protein metabolism and other cell activity but, in healthy cells, enzyme activity “defuses” them. Why this apparently doesn’t occur in ALS isn’t well-understood.

Yet much controversy has brewed over proving that this oxidative process is what truly causes the nerve cell insults of ALS. Although oxidative damage does in fact occur in the disease, some researchers believe it’s a secondary, downstream effect that doesn’t significantly reflect what goes awry due to the mutations.

Pioneering work by many of the Center’s investigators has looked into oxidative injury as a possible key mechanism for SOD1 toxicity. Because of these studies, they now downplay its importance.

Learn more about the research projects funded and coordinated by the Packard Center for ALS Research at Johns Hopkins, and targeted at finding the causes of ALS and a cure. Subscribe to ALS Alert to stay informed about ALS research and clinical trials.

From Our Experts

Current ALS Clinical Trials

  • Skin biopsies to generate cell lines for study of ALS

  • A Longitudinal Study of Cognition and Behavior in ALS

  • A Multicenter Study for the Validation of ALS Biomarkers

  • Electrical impedance myography as an outcome measure in ALS clinical trials

  • Quality of Life and Caregiver Burden in ALS

Johns Hopkins School of Medicine

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