SOD1 and amyotrophic lateral sclerosis: Due to the unknown genetic etiology of sporadic ALS, there are no transgenic animal models that correspond exactly to the human condition; however, we used a mouse model of familial ALS overexpressing mutant superoxide dismutase-1 (SOD1) with a guanine to alanine point mutation at amino acid 93, which exhibits neurodegeneration similar to human ALS [25,26].