In these diseases, misfolded or mutant variants of proteins such as tau and amyloid-β (Aβ) in AD9, huntingtin (HTT) in HD10, alpha-synuclein in PD and Lewy body dementia11, and TAR DNA-binding protein 43 (TDP-43), superoxide dismutase 1 (SOD1), optineurin (OPTN), fused in sarcoma (FUS), and ubiquilin-2 (UBQLN2) in ALS12, form protein aggregates and place increasing proteotoxic stress on the PQC pathways of the cells. This evidence concerns the gene HTT and Parkinson disease.