VPS35 and viral infectious disease: As viral infection has been shown to upregulate amyloidogenic α-synuclein species and cause deposition of aggregated α-synuclein [31,32,33], and D620N reduces the inhibitory effect of Vps35 on viral propagation, brain cells bearing Vps35D620N are prone to virus spread, which may plausibly increase the production of phosphorylated α-synuclein and lead to the deposition of α-synuclein aggregates.