During our study of miR-200a-3p on the pathological changes in AD associated with BACE1 and PRKACB, we explored the cell apoptosis, levels of Aβ1-42, and phosphorylation of the tau protein at several phosphorylated sites that PKA favors after overexpression of BACE1 and PRKACB cotransfected with miR-200a-3p mimics into APPswe cells. Here, PRKACB is linked to Alzheimer disease.