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Since human clinical trials are essentially nonexistent, the available data comes from anecdotal reports from the biohacking community

[29] Mouse models with this mutation do not exhibit the classical mitochondrial vacuolation pathology seen in G93A and G37R ALS mice and unlike G93A mice, deficiency of the major mitochondrial antioxidant enzyme, SOD2, has no effect on their disease course

On the other hand, if you dont have those, then youre focusing on other things

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Huynh P, Hoffmann JD, Gerhardt T, Kiss MG, Zuraikat FM, Cohen O, et al