These aggregates include β-amyloid (Aβ) in senile plaques and tau in neurofibrillary tangles (NFTs) in Alzheimer’s disease; α-synuclein in Lewy bodies and Lewy neurites in Parkinson’s disease; TAR-DNA-binding protein 43 (TDP-43) and superoxide dismutase (SOD1) aggregates in ALS; polyglutamine (polyQ)-rich huntingtin inclusions in Huntington’s disease and prion plaques in Creutzfeldt-Jakob disease (CJD). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.