Consistent with this, a report has described that LC3-II/LC3-I ratio reveals a decrease and p62 expression exhibits an increase in the cortex of AD mouse at the late stage of the disease, and the autophagosomes containing APP and Aβ are gathered in the axon and cannot be transported normally, thus disrupting the fusion of autophagosomes and lysosomes, and leading to the failure of Aβ degradation (Son et al., 2012; Bordi et al., 2016). The gene discussed is APP; the disease is Alzheimer disease.