BACE1 and Alzheimer disease: 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).