In summary, our study suggests that miR-200a-3p is implicated in AD progression and can exert neuroprotective effects against Aβ-induced toxicity by two possible mechanisms: first, by directly and/or indirectly inhibiting the overproduction of Aβ via suppressing the expression of BACE1 and second, by simultaneously decreasing the hyperphosphorylation of tau through attenuating the expression of PKA (Figure 6). This evidence concerns the gene MAPT and Alzheimer disease.