SOD1 and amyotrophic lateral sclerosis: Similar symptoms of ALS, including the loss ofclose synaptic contacts between motor neurons [1], disruption of the mitochondrial function [2], and activation of glial cells [3], have been confirmed inSOD1-trangenic mouse models expressing both dismutase-active(hSOD1G37R [4],hSOD1G93A [5]), and non-active(hSOD1G85R [6],hSOD1G127X [7]) mutants.Moreover, homozygous SOD1–deficient mice showed nosymptoms of neurodegenerative disorders [8].