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Confronting the rising tide of ischemic stroke and its associated mortality and morbidity with ageing, prevention and acute management of ischemic stroke is of paramount importance. Mounting observational studies have established a non-linear association of vitamin D status with cardiovascular diseases, including ischemic stroke. Paradoxically, current clinical trials fail to demonstrate the cardiovascular benefits of vitamin D supplementation. We aim to update recent clinical and experimental findings on the role of vitamin D in the disease course of ischemic stroke, from its onset, progression, recovery, to recurrence, and the established and alternative possible pathophysiological mechanisms. This review justifies the necessities to address stroke etiological subtypes and focus on vitamin D-deficient subjects for investigating the potential of vitamin D supplementation as a preventive and therapeutic approach for ischemic stroke. Well-powered clinical trials are warranted to determine the efficacy, safety, timing, target individuals, optimal dosages, and target 25OHD concentrations of vitamin D supplementation in the prevention and treatment of ischemic stroke., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Arterial stiffness index (ASI) is a potential risk factor for cerebrovascular and cardiometabolic diseases, but the causal links between them are inconclusive. The aim is to evaluate the causal effects of ASI on cerebrovascular and cardiometabolic diseases by Mendelian randomization (MR)., Methods: Two-sample MR analysis was performed to infer causal links. Genetic variants significantly associated with ASI were extracted. The inverse variance weighted method was used for estimating the effects. Sensitivity analysis was performed to test heterogeneity or pleiotropy., Results: MR analysis indicated an effect of genetically predicted ASI on the risk of ischemic stroke (IS) of all causes (OR = 1.894, 95% CI 1.210-2.965, p  = 0.005). No links were identified between genetically predicted ASI and other cerebrovascular or cardiometabolic diseases (all p  > 0.05). Subgroup analysis of IS etiologies found a suggestive association between genetically predicted ASI and large artery atherosclerosis stroke (LAS) (OR = 3.726, 95% CI 1.230-11.286, p  = 0.020). There were no effects of ASI on IS due to cardioembolism or small vessel occlusion., Conclusion: The current MR analysis suggested that genetically predicted ASI was associated with higher risk of IS of all causes. The results and the underlying pathways or mechanisms between ASI and IS needs further investigation.

Since metabolic dysregulation is a hallmark of both stroke and Alzheimer's disease (AD), mining shared metabolic patterns in these diseases will help to identify their possible pathogenic mechanisms and potential intervention targets. However, a systematic integration analysis of the metabolic networks of the these diseases is still lacking. In this study, we integrated single-cell RNA sequencing datasets of ischemic stroke (IS), hemorrhagic stroke (HS) and AD models to construct metabolic flux profiles at the single-cell level. We discovered that the three disorders cause shared metabolic shifts in endothelial cells. These altered metabolic modules were mainly enriched in the transporter-related pathways and were predicted to potentially lead to a decrease in metabolites such as pyruvate and fumarate. We further found that Lef1, Elk3 and Fosl1 may be upstream transcriptional regulators causing metabolic shifts and may be possible targets for interventions that halt the course of neurodegeneration. [ABSTRACT FROM AUTHOR]

Background: There is still no precise knowledge of the causes of progression in patients with acute ischemic stroke (AIS), and we are unable to predict patients at risk. Objective: To explore the frequency, predictive factors, and the prognosis of early neurological deterioration (END) in patients with AIS Methods: In this prospective multicenter observational study, we assessed patients with AIS admitted to 18 hospitals in Henan, China. We defined END as an increase of ⩾2 points in total National Institutes of Health Stroke Scale (NIHSS) score or ⩾1 point in the motor items of the NIHSS within 7 days after admission. Risk factors were analyzed using multivariate logistic regression models. Prognosis was evaluated using the modified Rankin Scale (mRS), with poor prognosis defined as mRS 3–6. Results: A total of 9114 patients with AIS within 24 h of symptom onset were enrolled in the study. END occurred in 1286 (14.1%) patients. The highest incidence (62.5%) of END occurred within 24 h after admission. After adjusting potential confounders, age, body mass index, waist–hip ratio, systolic blood pressure, baseline NIHSS, disabled at baseline, history of atrial fibrillation, diabetes mellitus, intracranial arterial stenosis, infarct location in the lenticulostriate artery area and cerebral watershed, neutrophils, lymphocytes, uric acid, and triglycerides were identified as independent predictors for END. END was significantly associated with poor prognosis at 90 days, and the adjusted OR was 1.74 (95% CI: 1.53–1.97). Conclusion: One in seven hospitalized patients with AIS may experience END within 24 h of onset. The highest incidence of END occurred within 24 h of admission and decreased steeply with time. Easily identifiable risk factors predict END and could help understand the causal mechanisms and thereby prevent END. [ABSTRACT FROM AUTHOR]