These diseases are attributed to the progressive deterioration of neuronal structure and functions [3], accompanied by the accumulation of misfolded proteins [4,5], such as amyloid-beta (Aβ) and tau in AD, alpha-synuclein (α-syn) in PD, mutant huntingtin (HTT) in HD, SOD1 and TDP-43 in ALS, and Epstein-Barr virus protein in MS. Here, SOD1 is linked to amyotrophic lateral sclerosis.