SOD1 and amyotrophic lateral sclerosis: The inhibition of mitochondrial fission by overexpression of inactivated Drp1 or Mfn2 prevents mitochondrial trafficking deficits in motor neurons expressing disease causing mutant SOD1 or TDP-43 [135,142], implying that, in addition to Miro1 deficiency, the mitochondrial fusion and fission dynamic abnormalities may also be responsible for impaired mitochondrial movement in ALS.