Much research has shown that the immune system and inflammation are likely involved in PD.105,203–207 Systemic inflammation is known to enhance infectivity of PrPSc, and subsequently, inflammation may also trigger and/or accelerate the infection and spread of prion α-synuclein.208,209 Specifically, gut inflammation may allow toxic luminal contents to diffuse across intestinal epithelial tight junctions,210 increase aggregation,209 and promote the spread of aggregates in the gut.209. Here, SNCA is linked to infection.