MicroRNAs (miRNAs) have multiple functions that regulate gene expression in various species. Few studies have explored the effects of miRNAs on the pathogenesis of Alzheimer's disease (AD); however, the potential neuroprotective effects of miRNAs on AD, particularly by targeting neuronal markers, remain unclear. In this study, we suggested potential neuroprotective roles for miR-937-3p in an in vitro AD model, which has not been extensively studied. Our biological analysis confirmed that miR-937-3p participated in neuronal protection and differentiation. We selected miR-937-3p as a novel candidate and identified Netrin1 (NTN1), an axon guidance regulator, as its target gene via qPCR analysis and luciferase assay. Additionally, FACS analysis revealed a reduction in apoptosis levels in Aβ-treated cells following treatment with the miR-937-3p-I. Western blot analysis showed that the expression of Mcl-1, an anti-apoptotic marker, increased with miR-937-3p-I treatment in an in vitro AD model. Interestingly, the levels of pro-caspase 7, pro-caspase 3, and pro-PARP, which are usually downregulated when their cleaved forms are upregulated, were found to increase with miR-937-3p-I treatment. The expression levels of neuronal markers such as NeuN, NFH, Tuj1, SYP, and MAP2 were enhanced by miR-937-3p-I treatment in the in vitro AD model. Therefore, miR-937-3p inhibition might play a therapeutic and neuroprotective role in AD by promoting NTN1 expression and repressing the apoptotic pathway.