Really, SALS and FALS are clinically indistinguishable suggesting a common pathogenesis of the disease; in fact, the protein products of genes associated with ALS as mutant SOD1, TDP43, or FUS were found in neuronal aggregates from ALS patients and observed to coincide with the manifestation of disease symptoms in all mouse models [16, 133] suggesting that, in addition to playing a role in FALS, these proteins may be altered also in SALS forms of the disease [134, 135]. Here, SOD1 is linked to amyotrophic lateral sclerosis.