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A proposed mechanism of ALS fails the test in vivo

In contrast to prevailing hypotheses, a genetic study shows that the toxic gain of function associated with mutant superoxide dismutase in familial amyotropic lateral sclerosis is unlikely to be due to changes in its oxidative activity causing an increase in free radicals.

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Figure 1: Aggregates of mutant SOD1 (G37R) protein in the neurites of lumbar spinal cord motor neurons accumulates even in the complete absence of CCS.

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Orr, H. A proposed mechanism of ALS fails the test in vivo. Nat Neurosci 5, 287–288 (2002). https://doi.org/10.1038/nn0402-287

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