APP and Alzheimer disease: Although no significant influence on Aβ production was observed in HT22 cells with miR-140/miR-122 overload, depletion of endogenous miR-140 and miR-122 by overexpressing miR-140-miR-122-TuD significantly reduced Aβ production in HT22, indicating a redundancy in APP processing and the therapeutic potentials of these miRNAs in AD treatment (Fig. 2J).