Effects of virtual reality cognitive training in individuals with mild cognitive impairment: A systematic review and meta-analysis.

BACKGROUND: Virtual reality (VR) is used to improve specific health needs by combining multiple technologies; it is increasingly being used in the medical field, showing satisfactory effects, especially in the management of chronic disease. The aim of this study was to assess the effects of VR cognitive training for individuals with mild cognitive impairment (MCI). METHODS: Peer-reviewed articles were searched from the PubMed, Embase, Web of Science, the Cochrane Library, Science Direct, and EBSCOhost databases, as well as CNKI, Sinomed, Vip. and Wan Fang, through 23 May 2021. We only included randomized controlled trials (RCTs) enrolling participants with MCI. RESULTS: Seventeen RCTs were included, with a total of 744 participants. Evidence of moderate quality showed that VR cognitive training significantly enhanced MCI patients' global cognitive function, as measured by the Montreal Cognitive Assessment (standardized mean difference [SMD] = 0.42; 95% confidence interval [CI], 0.04-0.79; p = 0.03) and executive function, as measured by trail making test A (SMD = -0.58; 95% CI, -0.80 to -0.35; p < 0.001). The meta-analysis indicated that the effects of VR cognitive training on delayed memory, immediate memory, attention and instrumental activities of daily living were not statistically significant (p > 0.05). CONCLUSION: The available data showed that VR cognitive training might be beneficial for improving global cognitive function and executive function in individuals with MCI, although the effects were short term.

TREM2 protects against cerebral ischemia/reperfusion injury.

Although post-ischemic inflammation induced by the innate immune response is considered an essential step in the progression of cerebral ischemia injury, the role of triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of ischemic stroke remains to be elucidated. Here, we found that the transcriptional and post-transcriptional levels of TREM2 were increased in cultured primary microglia after oxygen-glucose deprivation and reoxygenation and in the ischemic penumbra of the cerebral cortex after middle cerebral artery occlusion (MCAO) and reperfusion in mice. TREM2 was mainly expressed in microglia, but not in astrocytes, neurons, or oligodendrocytes in mice subjected to MCAO. Manipulating TREM2 expression levels in vitro and in vivo significantly regulated the production of pro- and anti-inflammatory mediators after ischemic stroke. TREM2 overexpression markedly suppressed the inflammatory response and neuronal apoptosis. By contrast, TREM2 gene silencing intensified the inflammatory response, increased neuronal apoptosis and infarct volume, and further exacerbated neurological dysfunction. Our study demonstrated that TREM2 protects against cerebral ischemia/reperfusion injury through the aspect of post-ischemic inflammatory response and neuronal apoptosis. Pharmacological targeting of TREM2 to suppress the inflammatory response may provide a new approach for developing therapeutic strategies in the treatment of ischemic stroke and other cerebrovascular diseases.