Wang L et al. [101] further found that the pathology of AD is associated with miR-200a-3p, which exerts neuroprotective effects against Aβ-induced toxicity through two possible mechanisms: one involves inhibiting Aβ overproduction by suppressing BACE1 expression, and the other involves attenuating PKA expression to reduce tau hyperphosphorylation. Here, BACE1 is linked to Alzheimer disease.