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Objective: There is a relationship between non-rapid eye movement (NREM) sleep and Alzheimer's disease (AD). The rostromedial tegmental nucleus (RMTg) is activated can enhance NREM. Therefore, our experiment was designed to investigate the effects of activation of RMTg by chemical genetic techniques on APP/PS1 mice learning and memory. Materials and Methods: After the AAV-hSyn-hM3Dq-mCherry virus was injected into the RMTg nucleus, CNO solution was intraperitoneally injected to activate RMTg. The new object test and Morris water maze were used to determine the learning and memory level; T2-weighted imaging (T2WI) scanning was performed to analyze the volume of hippocampus and entorhinal cortex of each group; The virus transfection status was determined by laser confocal microscope and use immunohistochemical detection to observe the deposition of Beta Amyloid 1-42 (Aß42). Results: Activation of RMTg by chemical genetic techniques can reduce the escape latency and increase discrimination index (RI) and the number of crossing platform; Activation of RMTg by chemical genetic techniques reduced the atrophy of the entorhinal cortex. Aß42 deposition in the brain was decreased after activation of RMTg. Conclusion: Activation of the RMTg nucleus by chemogenetic techniques can improve the learning and memory impairment in APP/PS1 mice.
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INTRODUCTION: Chronic ankle instability (CAI), which is characterized by deficient postural control, is associated with functional limitations and diminished self-reported quality of life. Recent studies have suggested that balance training can improve postural control, but high-quality evidence-based research to confirm the effect of balance training on dynamic postural stability in CAI patients is lacking. The purpose of this study was to synthesize current evidence regarding the effect of balance training on dynamic postural stability in CAI patients. EVIDENCE ACQUISITION: PubMed, Embase, Web of Science and Cochrane Library databases were searched for clinical trials that evaluated the effect of balance training on posture and balance in CAI patients from their inception to 15 July 2021. All statistical analyses were performed in RevMan 5.4. The risk of bias was assessed by the Cochrane Collaboration's risk of bias tool, and studies that reported statistically comparable outcomes were analyzed in meta-analyses using random effects models. Heterogeneity was assessed using the I2 statistic index. EVIDENCE SYNTHESIS: A total of 12 RCTs included in this meta-analysis and revealed that balance training was effective for improving the dynamic posture stability of CAI patients (SMD=0:90; 95% CI: 0.54 to 1.26; P<0:00001, I2=71%; Star Excursion Balance Test). Subgroup analysis (balance training vs. other training) revealed a small negative effect size, but this was not statistically significant (SMD=-0.12, 95% CI=-0.53 to 0.29, P=0.56, I2=9%). Another subgroup analysis (balance training vs. no training) revealed that balance training was more likely to have greater improvement on the dynamic posture stability of CAI patients (SMD=0.94, 95% CI: 0.71 to 1.17; P<0.00001, I2=0%). CONCLUSIONS: Balance training yielded a statistically significant and clinically meaningful improvement in dynamic postural stability in CAI patients. Limited evidence indicates that balance training was more effective than other training methods.
Subject(s)
Ankle Joint , Joint Instability , Humans , Ankle , Quality of Life , Randomized Controlled Trials as Topic , Postural Balance , Chronic DiseaseABSTRACT
The changes of neurochemicals in mild cognitive impairment (MCI) and Alzheimer's disease (AD) patients has been observed via magnetic resonance spectroscopy in several studies. However, whether it exists the consistent pattern of changes of neurochemicals in the encephalic region during the progression of MCI to AD were still not clear. The study performed meta-analysis to investigate the patterns of neurochemical changes in the encephalic region in the progress of AD. We searched the PubMed, Embase, Cochrane Library, and Web of Science databases, and finally included 63 studies comprising 1,086 MCI patients, 1,256 AD patients, and 1,907 healthy controls. It showed that during the progression from MCI to AD, N-acetyl aspartate (NAA) decreased continuously in the posterior cingulate (PC) (SMD: -0.42 [95% CI: -0.62 to -0.21], z = -3.89, P < 0.05), NAA/Cr (creatine) was consistently reduced in PC (SMD: -0.58 [95% CI: -0.86 to -0.30], z = -4.06, P < 0.05) and hippocampus (SMD: -0.65 [95% CI: -1.11 to -0.12], z = -2.44, P < 0.05), while myo-inositol (mI) (SMD: 0.44 [95% CI: 0.26-0.61], z = 4.97, P < 0.05) and mI/Cr (SMD: 0.43 [95% CI: 0.17-0.68], z = 3.30, P < 0.05) were raised in PC. Furthermore, these results were further verified by a sustained decrease in the NAA/mI of PC (SMD: -0.94 [95% CI: -1.24 to -0.65], z = -6.26, P < 0.05). Therefore, the levels of NAA and mI were associated with the cognitive decline and might be used as potentially biomarkers to predict the possible progression from MCI to AD. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42020200308.
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The purpose of the present study was to evaluate the effect of electroacupuncture (EA) on the axonal regeneration environment following cerebral ischemia injury and to investigate whether it was associated with Nogo-A/Nogo receptor (NgR)/RhoA/Rho-associated protein kinase (ROCK) signaling. Using a rat model of focal cerebral ischemia, the effects of EA at the Quchi (LI11) and Zusanli (ST36) acupoints on axonal growth inhibitory protein and axonal growth factors were assessed and the underlying molecular mechanisms were investigated. It was found that EA at the Quchi and Zusanli acupoints significantly improved neurological deficit scores following ischemia (P<0.05), and reduced the cerebral infarct volume. Moreover, it was demonstrated that crucial signaling molecules in the Nogo-A signaling pathway were regulated by EA. These results suggest that EA provides a less inhibitory environment for axonal regeneration following cerebral ischemia through inhibition of Nogo-A/NgR/RhoA/ROCK signaling.
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BACKGROUND/AIMS: Recently, it has been reported that the microRNA-132(miR-132) is linked with synaptic plasticity and cognitive impairment. The present study investigates that whether miR-132 is altered in circulating blood serum samples of post-stroke cognitive impairment (PSCI) patients. METHODS: We collected samples from 39 subjects with PSCI, 37 subjects with post-stroke cognitive normality (PSCN), and 38 age-matched controls (AMC) for which ages, gender and education level were matched. MiR-132 was detected using a quantitative real-time PCR (qRT-PCR) method. To test the predictive value of miR-132 for PSCI, prediction capabilities were compared using the receiver operating characteristic (ROC) curves and area under curve (AUC) analysis. RESULTS: The level of miR-132 in PSCI patient serum was significantly elevated compared to that of PSCN and AMC subjects. The ROC curve showed that miR-132 achieved an AUC of 0.961 (p<0.0001). Importantly, the miR-132 level was correlated with the Montreal Cognitive Assessment (MoCA) score in PSCI patients. CONCLUSIONS: These results indicated that there was a substantial correlation between serum miR-132 expression and post-stroke cognitive functionality, suggesting that miR-132 may be a risk marker for PSCI. Because of the limitations of this study, the results should be treated with caution.
