Moreover, altered presynaptic inputs to MNs have been observed upon accumulation of mutant SOD1 [32], indicating that the presence of the aggregation-prone form of the protein product of ALS genes might represent a common trigger of synaptic alterations and contribute to the accumulation of regulatory proteins due to impaired catabolism [14, 70]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.