Conclusions

In the twelve years since the link between mutations in SOD1 and ALS was first identified, enormous amounts of research effort have been invested to understand the molecular basis for this deadly disease. It is clear that there are many factors involved in the pathogenesis of ALS, and it is becoming increasingly evident that researchers are unlikely to find the answer in one factor alone. Based on the data reviewed here, metal deficiency likely plays a substantial role in the propensity for protein aggregation, either through dimeric or monomeric forms. As our understanding of the molecular basis for pathogenic SOD1 expands, the research community looks forward to the application of this knowledge into prospective therapies for the disease.

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