ObjectiveStroke is a leading cause of death and disability worldwide. Neuroprotective approaches have failed in clinical trials, thus warranting therapeutic innovations with alternative targets. The gut microbiota is an important contributor to many risk factors for stroke. However, the bidirectional interactions between stroke and gut microbiota remain largely unknown.DesignWe performed two clinical cohort studies to capture the gut dysbiosis dynamics after stroke and their relationship with stroke prognosis. Then, we used a middle cerebral artery occlusion model to explore gut dysbiosis post-stroke in mice and address the causative relationship between acute ischaemic stroke and gut dysbiosis. Finally, we tested whether aminoguanidine, superoxide dismutase and tungstate can alleviate post-stroke brain infarction by restoring gut dysbiosis.ResultsBrain ischaemia rapidly induced intestinal ischaemia and produced excessive nitrate through free radical reactions, resulting in gut dysbiosis with Enterobacteriaceae expansion. Enterobacteriaceae enrichment exacerbated brain infarction by enhancing systemic inflammation and is an independent risk factor for the primary poor outcome of patients with stroke. Administering aminoguanidine or superoxide dismutase to diminish nitrate generation or administering tungstate to inhibit nitrate respiration all resulted in suppressed Enterobacteriaceae overgrowth, reduced systemic inflammation and alleviated brain infarction. These effects were gut microbiome dependent and indicated the translational value of the brain–gut axis in stroke treatment.ConclusionsThis study reveals a reciprocal relationship between stroke and gut dysbiosis. Ischaemic stroke rapidly triggers gut microbiome dysbiosis with Enterobacteriaceae overgrowth that in turn exacerbates brain infarction.

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White matter (WM) disease is recognized as an important cause of cognitive decline and dementia. White matter lesions (WMLs) appear as white matter hyperintensities (WMH) on T2-weighted magnetic resonance imaging (MRI) scans of the brain. Previous studies have shown that type 2 diabetes (T2DM) is associated with WMH. In this review, we reviewed the literature on the relationship between T2DM and WMH in PubMed and Cochrane over the past five years and explored the possible links among the presence of T2DM, the course or complications of diabetes, and WMH. We found that: (1) Both from a macro- and micro-scopic point of view, most studies support the relationship of a larger WMH and a decrease in the integrity of WMH in T2DM; (2) From the relationship between brain structural changes and cognition in T2DM, the poor performance in memory, attention, and executive function tests associated with abnormal brain structure is consistent; (3) Diabetic microangiopathy or peripheral neuropathy may be associated with WMH, suggesting that the brain may be a target organ for T2DM microangiopathy; (4) Laboratory markers such as insulin resistance and fasting insulin levels were significantly associated with WMH. High HbA1c and high glucose variability were associated with WMH but not glycemic control.

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Introduction Only two studies investigated the associations between peak width of skeletonized mean diffusivity (PSMD) and age‐related cognitive alterations, whereas none of the studies investigated the association with vascular risk factors. Methods We evaluated 801 stroke‐ and dementia‐free elderlies with baseline and 3‐year follow‐up assessments. Regression analyses were used to assess the association between age‐related cognitive functions and PSMD. Simple mediation models were used to study the mediation effect of PSMD between vascular risk factors and age‐related cognitive outcomes. Results PSMD was negatively associated with processing speed at baseline and negatively associated with processing and memory scores at 3‐year follow‐up. The association between vascular risk factors and age‐related cognition was mediated by PSMD, as well as other diffusion tensor imaging markers. Discussion PSMD is preferred over other diffusion tensor imaging markers as it is sensitive to age‐related cognitive alterations and calculation is fully automated. PSMD is proposed as a research tool to monitor age‐related cognitive alterations.

Backgrounds: Cognitive functions (CF) decline has been reported in end-stage renal disease (ESRD) patients. However, the influence of dialysis modalities on CF has not been investigated systematically. Methods: A systematic literature search was conducted in MEDLINE, Embase, Cochrane library and unpublished database Clinicaltrials.gov to identify the studies comparing the cognitive functions or risk of dementia between hemodialysis (HD) and peritoneal dialysis (PD). After data extraction, quality of studies was assessed using the Newcastle-Ottawa scale. Both qualitative and quantitative analyses were performed. Results: After study inclusion, totally 15 cohort or cross-sectional studies were included, comparing the cognitive functions using neuropsychological tests and covering the executive function, memory, orientation, attention, etc. By qualitative analysis, it showed that more studies are inclined to PD compared with HD with better cognitive functions. By quantitative analysis, it showed that PD showed better performance in the tests of Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), stroop interference test and exhibited lower risk of dementia compared with HD. Conclusions: In this meta-analysis, we draw preliminary conclusion that patients treated with PD had better cognitive functions and lower dementia risk compared with patients with HD. Still more large-scale and well-conducted prospective cohort studies are needed to draw more convincing conclusions.

Purpose: Stroke-associated infection (SAI) is associated with adverse outcomes in patients with acute ischemic stroke (AIS). In this study, we aimed to evaluate the association between neutrophil percentage-to-albumin ratio (NPAR) and SAI occurrence in patients with AIS.Methods: We retrospectively analyzed all AIS patients who were admitted to the Neurology ward of The Second Hospital of Tianjin Medical University from November 2018 to October 2020. The relationship between NPAR and SAI was analyzed by multivariable analysis. The receiver operating characteristic (ROC) curve was used to compare the predicted value of albumin, neutrophil percentage, neutrophil-to-lymphocyte ratio (NLR), and NPAR.Results: We included 379 AIS patients out of which 51 (13.5%) developed SAI. The NPAR was independently associated with increased risk of SAI adjusting for confounders [adjusted odds ratio (aOR) = 10.52; 95% confidence interval (CI), 3.33–33.28; P <0.001]. The optimal cutoff value of NPAR for predicting SAI incidence was 1.64, with sensitivity and specificity of 90.2 and 55.8%, respectively. The area under the curve (AUC) value of NPAR [0.771 (0.725–0.812)] was higher than that of albumin [0.640 (0.590–0.689)], neutrophil percentage [0.747 (0.700–0.790)], and NLR [0.736 (0.689–0.780)], though the statistical significance appeared only between NPAR and albumin.Conclusions: We demonstrated that a higher NPAR could predict the occurrence of SAI. Thus, NPAR might be a more effective biomarker to predict SAI compared with albumin, neutrophil percentage, and NLR.

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