Abstract. MicroRNAs (miRs) are a class of endogenous small non-coding RNAs that have been revealed to negatively mediate the expression of their target genes at the post-transcriptional level. Recently, particular miRs have demonstrated an involvement in the pathogenesis of Alzheimer's disease (AD). However, the specific role of miR-135b in AD has yet to be elucidated. The present study aimed to investigate the neuroprotective role of miR-135b, in addition to its underlying mechanism. Herein, reverse transcription-quantitative polymerase chain reaction was conducted to determine miR-135b expression levels in the peripheral blood samples of patients with AD and age-matched normal controls. The data of the present study revealed that the expression levels of miR-135b were significantly reduced in the peripheral blood of AD patients compared with normal controls (P<0.01). In vitro MTT analyses identified that the overexpression of miR-135b significantly enhanced the proliferation of hippocampal cells (P<0.01). Furthermore, in vivo analysis using a Y-maze test indicated that injection with miR-135b mimics into the third ventricle of anesthetized SAMP8 mice significantly enhanced their learning and memory capacities (P<0.01). Molecular mechanism investigations identified β-site APP-cleaving enzyme 1 (BACE1) as a direct target gene of miR-135b, and the latter was identified to negatively mediate the protein expression levels of BACE1 in hippocampal cells, in addition to hippocampal tissues, of SAMP8 mice. Based on the aforementioned findings, we propose that miR-135b has a neuroprotective role via direct targeting of BACE1 and, thus, may be used for the treatment of AD.

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Activated microglia are capable of facilitating amyloid-β (Aβ) accumulation via the release of inflammatory factors, thus resulting in the exacerbation of Alzheimer's disease (AD). MicroRNAs (miRs) participate in the activation of microglia, which is associated with AD. Insulin-like growth factor 1 (IGF1) is a neuroprotective, anti-inflammatory factor, which is able to accelerate clearance of Aβ peptides. The present study aimed to investigate the precise role of miR‑206 and IGF1 in lipopolysaccharide (LPS)‑induced microglial inflammation. The expression levels of miR‑206 and IGF1 were detected in 60 peripheral blood samples from patients with AD and matched age subjects using quantitative polymerase chain reaction. A dual luciferase reporter gene assay was used to indicate the relationship between miR‑206 and IGF1. In addition, the role of miR‑206 was determined by gain and loss of function experiments in LPS‑treated microglia. The results demonstrated that miR‑206 upregulation enhanced LPS‑induced inflammation and Aβ release in microglia by directly targeting the 3'-untranslated region of IGF1. These effects were attenuated following treatment with exogenous IGF1, thus indicating that the miR‑206/IGF1 signaling pathway may be considered a novel therapeutic target for the treatment of AD‑associated microglial inflammation.

To evaluate the association between plasma levels of copeptin and 1-year mortality in a cohort of Chinese patients with acute ischemic stroke. We prospectively studied 275 patients with ischemic stroke who were admitted within 24 h after the onset of symptoms. Copeptin and NIH stroke scale (NIHSS) score were measured at the time of admission. The prognostic value of copeptin to predict mortality within 1 year was compared with the NIHSS score and other known outcome predictors. Nonsurvivors had significantly higher copeptin levels on admission compared with survivors (P<0.0001). Multivariate logistic regression analysis showed that elevated plasma levels of copeptin were an independent stroke mortality predictor, with an adjusted odds ratio of 4.48 [95% confidence interval (CI), 2.18-9.06]. The area under the receiver operating characteristic curve of copeptin was 0.882 (95% CI, 0.847-0.921) for stroke mortality, which yielded a sensitivity of 90.7% and a specificity of 84.5%. Copeptin improved the NIHSS score (area under the curve of the combined model, 0.94; 95% CI, 0.91-0.97; P=0.011). Elevated plasma copeptin levels at admission were an independent predictor of long-term mortality after ischemic stroke in a Chinese sample, suggesting that these alterations might play a role in the pathophysiology of stroke.

Natural disasters cause long-term psychological problems and increase substance use in some adults. However, it is unclear whether disasters also lead to these problems in adolescents. We hypothesized the influence of adolescent resilience on mobile phone addiction during the normalization of COVID-19 and flooding. We tested the mediating role of coping style and depression, anxiety, and stress (DASS) on phone addiction among 1,751 adolescents in the Henan Province in China. The adolescents were surveyed via an online questionnaire, and we used structural equation modeling to examine the correlations and moderation effects. The results show that coping style and DASS could mediate the relationship between adolescent resilience and mobile phone addiction among Chinese adolescents. A chain of coping styles and DASS mediated the relationship between adolescent resilience and mobile phone addiction in Chinese adolescents.