SOD1 and amyotrophic lateral sclerosis: Using the transgenic mouse model SOD1G93A (SOD, Gly93→Ala substitution), which expresses a large degree of human mutant SOD1 and faithfully recapitulates a vast majority of the pathology’s abnormalities seen in ALS patients (Fogarty, 2018), we previously found that SOD MNs are hyperexcitable at the prenatal (embryonic day (E) 17.5) stage because of a shorter dendritic tree and increased input resistance (Martin et al., 2013).