In particular, by studying a mouse model of MPS-IIIA, we have shown that brain deposition of α-synuclein together with other amyloidogenic proteins including tau, Aβ, and PrP trigger neurodegenerative processes by both loss-of-function (LOF) (Sambri et al., 2017) and gain of toxic function mechanisms (Monaco et al., 2020) (see next sections for further discussion). Here, SNCA is linked to mucopolysaccharidosis type 3A.