CTSS and Alzheimer disease: Once generated, Aβ can be degraded by cathepsins in lysosomes (Miners et al., 2011) and the remaining Aβ can either accumulate in endolysosomes where it may precipitate AD pathogenesis (Braak and Del Tredici, 2004; LaFerla et al., 2007; Zou et al., 2015) or it can be released via exocytosis (Annunziata et al., 2013; Nilsson et al., 2013).