ObjectiveCurrently, the prevalence of CF (Cognitive Frailty) is not very clear, and the relationship between CF and its associated risk factors has not been accurately evaluated. Therefore, it is necessary to conduct a systematic review and meta-analysis further to understand CF's prevalence and associated factors.MethodsEmbase, PubMed, Web of Science, Ovid, and Cochrane were systematically searched for articles exploring the prevalence of CF, the deadline of searching date was up to March 2021. For the prevalence of CF, the events of CF and the total number of patients in every included study were extracted to estimate the prevalence of CF. For associated factors of CF, Odds Ratios (ORs) with (corresponding) 95% confidence intervals (CIs) were used for estimations.ResultsFirstly, the estimated prevalence of CF I (Cognitive Frailty in the model I) was 16%, 95% CI (0.13–0.19), and the estimated prevalence of CF II (Cognitive Frailty in model II) was 6%, 95% CI (0.05–0.07). Secondly, both lower engagement in activities and age were calculated to be independent risk factors of CF, and the OR (95% CI) was 3.31 (2.28–4.81) and 1.10 (1.04–1.16), respectively. Finally, depression was also a prominent risk factor of CF, with the overall OR (95% CI) as 1.57 (1.32–1.87).ConclusionCF was a high prevalence in community older. The various assessment scales and the different cutoff values of diagnostic criteria would affect the prevalence of CF. Lower engagement in activities, age, and depression was the risky factor of CF.Systematic Review Registrationhttp://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42019121369.

PurposeAlzheimer's disease (AD) is the sixth most common cause of death in the United States. MicroRNAs have been identified as vital players in neurodegenerative diseases, including AD. microRNA-128 (miR-128) has been shown to be dysregulated in AD. This study aimed to explore the roles and molecular mechanisms of miR-128 in AD progression.Materials and MethodsExpression patterns of miR-128 and peroxisome proliferator-activated receptor gamma (PPAR-γ) messenger RNA in clinical samples and cells were measured using RT-qPCR assay. PPAR-γ protein levels were determined by Western blot assay. Cell viability was determined by MTT assay. Cell apoptotic rate was detected by flow cytometry via double-staining of Annexin V-FITC/PI. Caspase 3 and NF-κB activity was determined by a Caspase 3 Activity Assay Kit or NF-κB p65 Transcription Factor Assay Kit, respectively. Bioinformatics prediction and luciferase reporter assay were used to investigate interactions between miR-128 and PPAR-γ 3′UTR.ResultsMiR-128 expression was upregulated and PPAR-γ expression was downregulated in plasma from AD patients and amyloid-β (Aβ)-treated primary mouse cortical neurons (MCN) and Neuro2a (N2a) cells. Inhibition of miR-128 decreased Aβ-mediated cytotoxicity through inactivation of NF-κB in MCN and N2a cells. Moreover, PPAR-γ was a target of miR-128. PPAR-γ upregulation attenuated Aβ-mediated cytotoxicity by inactivating NF-κB in MCN and N2a cells. Furthermore, PPAR-γ downregulation was able to abolish the effect of anti-miR-128 on cytotoxicity and NF-κB activity in MCN and N2a cells.ConclusionMiR-128 inhibitor decreased Aβ-mediated cytotoxicity by upregulating PPAR-γ via inactivation of NF-κB in MCN and N2a cells, providing a new potential target in AD treatment.

Study design Experimental animal study. Objectives To validate the anti-apoptosis effect of microRNA-21 in neurons after spinal cord injury (SCI) and explore the mechanism. Setting Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China. Methods In situ hybridization was used to detect the expression of miR-21 in spinal cord neurons (n = 24). In a rat contusion SCI model (n = 48), we upregulated the miR-21 level around the injured area using miR-21 lentiviral vectors and evaluated the therapeutic effect with histology and behavioural scores. In neuronal cells, oxygen-glucose deprivation (OGD) was exerted to imitate SCI, and we explored the biomechanism using molecular biology and a dual-luciferase reporter assay. Results miR-21 was expressed in spinal cord neurons and was found to improve neuronal survival and promote functional recovery in rat SCI models. The in vitro results in PC-12 cells revealed that the augmentation of endogenous miR-21 was able to reduce neuronal cell death after OGD. In addition, overexpression of miR-21 was able to reduce cellular apoptosis via decreasing PDCD4 protein levels, and caspase-3 activity was also influenced. Transfection of miR-21 into 293T cells was able to decrease luciferase activity in a reporter assay system, including the 3′ untranslated region of PDCD4. Conclusions miR-21 may have a protective role in neuronal apoptosis after SCI. PDCD4 may be a functional target gene involved in the miR-21-mediated anti-apoptotic effect through an miR-21/PDCD4/caspase-3 pathway.

No abstract