One of the hallmarks of Alzheimer's disease is the accumulation of amyloid-β (Aβ) plaques (Stelzmann et al., 1995); Aβ is a cleavage product of endosome-associated processing of APP (Reiss et al., 2018), a membrane-bound, secreted protein that is known to undergo retromer-dependent retrograde trafficking via recycling of the Sortilin-LA (SorLA; also known as SORL1) sorting receptor (Fjorback et al., 2012; Lane et al., 2012; Wang and Bellen, 2015). This evidence concerns the gene APP and Alzheimer disease.