Amyotrophic Lateral Sclerosis (ALS) is characterized by selective degeneration of motor neurons, which is linked to excitotoxicity (defect of AMPA receptor function), increase in Ca2+ influx, decrease in excitatory amino acid transporter 2 (EAAT-2) levels, mutation of SOD1 and defect of mitochondrial ETC complex IV, ultimately leading to oxidative stress and motor neuron death [17]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.