SOD1 and amyotrophic lateral sclerosis: Though an ideal control for the G93A*SOD1 mice would be a transgenic mouse overexpressing human wildtype SOD1 (SOD1Wt), several studies reported that SOD1Wt mice develop ALS-like phenotype and other neuronal dysfunction [34,35] and therefore, cannot be used as a control of mutant SOD1 experiments.