Exogenous amyloids of the various causative proteins of these diseases (Aβ42 and tau for AD, polyQ repeat expansions in Huntingtin, α-synuclein for PD, and SOD1 for ALS) induce misfolding of their naturally structured counterparts in cells, tissues, and animal models. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.