Deficiency in VPS35/retromer has been observed in the hippocampus of AD patients, while deficiencies in the retromer components VPS35 and SNX6 can promote Aβ biogenesis by prolonging APP retention in early endosomes and facilitating retrograde transport of BACE1 from endosomes to TGN, respectively [154–156]. Here, VPS35 is linked to Alzheimer disease.