(APP) to the pro-aggregatory neurotoxic Aβ peptide (Small et al., 2005; Muhammad et al., 2008). Variants of the Snx3 and Rab7a genes required for the recruitment of the retromer CSC are linked to late-onset AD and hence retromer function has been of interest to researchers investigating the underlying causes of AD (Vardarajan et al., 2012; Small, 2008). Indeed it has been shown that a pharmacological chaperone that can bind to VPS35 at the VPS35-VPS29 interface enhances the stability of the retromer CSC increasing levels in neuronal cells and reducing the processing of APP to Aβ (Mecozzi et al., 2014).
