Atherosclerosis (AS) is a common vascular disease with great harm. The current study examined the expression pattern of miR-18a-5p in AS patients, and explored its clinical values. 110 AS patients and 68 healthy controls were collected clinically, and the expression pattern of miR-18a-5p in the serum of AS patients was detected using qRT-PCR. All AS patients were followed up for five years to record the adverse cardiovascular events. ROC and Kaplan-Meier (K-M) curve were plotted to assess the diagnostic ability. The multiple Cox regression analysis was performed for independent influencing factors analysis. MiR-18a-5p was at high expression in AS patients, and showed positive correlation with the CIMT value ( r = 0.789, P < .001). ROC curve suggested the high diagnostic value of serum miR-18a-5p for AS, with the AUC of 0.894. The diagnostic specificity and sensitivity were 86.8% and 79.1%, respectively. K-M plot demonstrated that cases with high miR-18a-5p levels were more likely to suffer from cardiovascular events, and it is an independent influence factor for the poor clinical outcome. Serum miR-18a-5p serves as a promising biomarker for AS diagnosis, and is related to the occurrence of adverse cardiovascular events.

<b><i>Introduction:</i></b> This study aimed to explore the diagnostic value and effect of miR-381-3p on Alzheimer’s disease (AD). <b><i>Methods:</i></b> RT-qPCR was used for the measurement of miR-381-3p levels. Pearson correlation coefficient was used for the correlation analysis. Receiver operating characteristic (ROC) curve was constructed to assess the distinct ability of miR-381-3p for AD. SH-SY5Y cells were treated with Aβ25-35 to establish an AD cell model. The role of miR-381-3p on cell proliferation and apoptosis was detected. ELISA was applied to detect the protein levels of inflammatory cytokine expression. The target relationship of miR-381-3p with PTGS2 was verified by luciferase reporter gene assay. <b><i>Results:</i></b> Low expression of miR-381-3p was detected in the serum of AD patients and cell models. There was a negative association of serum miR-381-3p with the serum inflammatory cytokines. The ROC curve demonstrated the distinct ability of serum miR-381-3p for AD, with the AUC value of 0.898, with a sensitivity of 87.5%, and a specificity of 77.7%. Overexpression of miR-381-3p reversed the influence of Aβ25-35 on cell proliferation and apoptosis, but miR-381-3p downregulation exacerbated the influence. miR-381-3p overexpression inhibited the release of IL-6, IL-1β, and TNF-α induced by Aβ25-35 treatment, whereas miR-381-3p downregulation further promoted the release of inflammatory cytokines. PTGS2 was the target gene of miR-381-3p and was upregulated in AD cell models. <b><i>Conclusion:</i></b> miR-381-3p is less expressed in the serum of AD patients and has potential diagnostic values for AD. Overexpression of miR-381-3p may attenuate Aβ25-35-induced neurotoxicity and inflammatory responses via targeting PTGS2 in SH-SY5Y cells.