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Alzheimer’s disease is the most common dementia disease characterized by chronic progressive neurodegeneration. The incidence of Alzheimer’s disease is on the rise as the population ages at an accelerating pace. According to epidemiological data, by 2050, the number of Alzheimer’s patients in the United States will be three times higher than that in 2010, and a similar trend is occurring in China. To explore the effect and mechanism of let-7b by detecting the expression level of let-7b in Alzheimer’s disease, fifty patients with Alzheimer’s disease and thirty healthy controls were selected. The expression levels of let-7 families (let-7a, let-7b, let-7c, let-7d, let-7e, let-7f, let-7g, and let-7i) were detected by qPCR. Human neuroblastoma cell SK-N-SH were divided into control group (untreated), model group (treated with Aβ1-40), Aβ1-40+let-7b mimic group (treated with Aβ1-40 and transfected with let-7b mimic), and Aβ1-40+miR-NC group (treated with aβ1-40 and transfected with miR-NC). let-7b expression and cell survival rate were detected by qPCR and CCK-8, and the levels of caspase 3, LC3, beclin-1, PI3K, p-AKT, and p-mTOR were detected by Western blot. let-7b was significantly different between the case group and the control group ( p  &lt; 0.001). CCK-8 showed a significant decrease in cell viability in Aβ1-40 treatment group compared with that in the control group ( p  &lt; 0.01). Overexpression of let-7b significantly reduced the survival rate of the cells, and the expression of LC3II/LC3I and beclin-1 in the cells was significantly reduced by aβ1-40 treatment ( p  &lt; 0.001). let-7b overexpression also inhibited autophagy via reducing the level of LC3II/LC3I and beclin-1 ( p  &lt; 0.001). Aβ1-40 treatment and let-7b overexpression promoted apoptosis by increasing the expression of cleavage caspase 3. Western blot indicated that Aβ1-40 treatment and let-7b overexpression could increase the expression of PI3K, p-AKT, and p-mTOR. let-7b overexpression could inhibit autophagy and promote apoptosis in Alzheimer’s cells by promoting PI3K/AKT/mTOR signaling pathway. PI3K/AKT/mTOR signaling pathway is involved in the imbalance between autophagy and apoptosis.

Inhibiting Autophagy Pathway of PI3K/AKT/mTOR Promotes Apoptosis in SK-N-SH Cell Model of Alzheimer’s Disease