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New Findings: What is the central question of this study?What is the mechanism of miR‐211 in an Alzheimer's disease cell model?What is the main finding and its importance?miR‐211 was upregulated in an Alzheimer's disease cell model. It targeted neurogenin 2, reduced the activation of the phosphoinositide 3‐kinase–Akt signalling pathway, inhibited the proliferation of the Alzheimer's disease cell model and promoted apoptosis. MicroRNAs (miRs) are aberrantly expressed in Alzheimer's disease (AD) patients. This study was intended to investigate the effect of miR‐211 on an AD cell model and the involvement of neurogenin 2 (Ngn2). The appropriate dose and time for the effect of Aβ1–42 on PC12 cells were determined to establish an AD cell model. An effect of miR‐211 expression on cell viability, proliferation and apoptosis was detected after cell transfection. Online prediction and a dual luciferase reporter gene assay were utilized to confirm the binding sequence of miR‐211 and Ngn2. qRT‐PCR and western blot analysis were applied to measure Ngn2 expression. A gain and loss of function assay of miR‐211 and Ngn2 was performed, and activation of the phosphoinositide 3‐kinase (PI3K)–Akt signaling pathway was detected. The AD cell model was induced by Aβ1–42 treatment. miR‐211 expression was significantly enhanced after miR‐211 transfection, leading to suppressed proliferation and promotion of apoptosis in Aβ1–42‐treated PC12 cells. In addition, miR‐211 could downregulate Ngn2 mRNA and protein expression, while overexpression of Ngn2 could reverse the effects of miR‐211 on Aβ1–42‐treated PC12 cells and significantly enhance the phosphorylated Akt and PI3K protein levels. miR‐211 could inhibit growth of PC12 cells by suppressing Ngn2 expression and inactivating the PI3K–Akt signalling pathway. [ABSTRACT FROM AUTHOR]