One hypothesis is that early AD-associated defects in secretory pathways, which release cleaved forms of APP including Aβ-peptides, disrupt neuronal cell biology, altering processes such as endolysosomal trafficking, thus progressively leading to cell death (Kimura and Yanagisawa, 2018; Cataldo et al, 2000; Weglinski and Jeans, 2023). The gene discussed is APP; the disease is Alzheimer disease.