In AD, dysfunctional autophagic flux was characterized as accumulating levels of APs in dystrophic neurites, whereas APP, Aβ peptides, β-site APP cleaving enzyme (BACE1) protein, damaged mitochondria and Golgi fragments are rich and cannot be cleared away by endosomal–lysosomal degradation process (Yu et al., 2005; Joshi and Wang, 2015; Feng et al., 2017; Kerr et al., 2017; Nixon, 2017). The gene discussed is BACE1; the disease is Alzheimer disease.