Since emerging evidence suggests that the pathogenesis of AD involves mitochondrial dysfunction, oxidative stress damage, calcium homeostasis and inflammation (Scheltens et al., 2016; Cheignon et al., 2018; Lee et al., 2018), we have proposed that opioid receptors may play a role in the pathology of AD, including regulations of the BACE1-mediated Aβ production with δ-opioid receptor (DOR) being neuroprotective. This evidence concerns the gene BACE1 and Alzheimer disease.