BACE1 and Alzheimer disease: In conclusion, our study suggests that miR-200a-3p is implicated in the pathology of AD, exerting neuroprotective effects against Aβ-induced toxicity by two possible mechanisms: one involving the inhibition of Aβ overproduction via suppression of the expression of BACE1 and synergistically decreasing the hyperphosphorylation of tau via attenuation of the expression of PKA.