Indeed, protein aggregates are a hallmark of Alzheimer’s disease, in which amyloid beta peptides form toxic plaques, and hyperphosphorylated tau proteins accumulate into neurofibrillary tangles, Parkinson’s disease, in which α-synuclein is seen to form characteristic Lewy bodies, and ALS in which mutant and oxidized forms of various proteins, particularly SOD1 and TAR-DNA-binding protein-43 (TDP-43) among others, have been shown to forms large aggregates throughout the cell (Table 1). This evidence concerns the gene SOD1 and Parkinson disease.