Meilandt et al. (2008) previously reported that the irreversible blockade of MOR with β-funaltrexamine ameliorated memory deficits induced by human amyloid precursor protein expressed in transgenic mice. Our results and their observation support each other in terms of MOR’s role in AD pathology. Since DADLE is not a specific ligand for DOR (Blurton et al., 1986; Xia, 2015), its side action on MOR is likely the reason for DADLE-induced upregulation of BACE1 expression and activity as shown in the previous reports (Ni et al., 2006; Teng et al., 2010). This evidence concerns the gene BACE1 and Alzheimer disease.