In addition to α-synuclein misfolding and aggregation, other cell and tissue alterations underlie the initiation and progression of PD, including mitochondrial dysfunction [20], altered protein clearance (involving ubiquitin-proteasome) [21] and autophagy-lysosomal systems [22], neuroinflammation (to which autoimmunity may contribute [23]), and oxidative stress [24,25]. Here, SNCA is linked to Parkinson disease.