SOD1 and amyotrophic lateral sclerosis: There is growing evidence that protein aggregation, such as extracellular accumulation of amyloid-β (Aβ) and intraneuronal hyperphosphorylated tau in AD, synaptic protein α-synuclein deposition (referred to as Lewy bodies) in the neuronal cells in PD, and expanded polyglutamine (polyQ) accumulation in HD and ALS involving the inclusion of SOD1, TDP-43, and FUS, induce neuronal loss through a toxic gain of function [22,23,24,25,26].