Objective: To investigate the impact of N-terminal pro-B-type natriuretic peptide (NT-proBNP) on CTP infarct core volume and poor 90-day functional outcomes in acute ischemic stroke (AIS). Methods: A total of 403 hospitalized patients with AIS in the Stroke Center of the First Hospital Affiliated to Soochow University were enrolled from March 2018 to January 2021. The association between NT-proBNP and clinical outcomes in acute ischemic patients was assessed by logistic regression and adjusted for confounding factors. Also, subgroup analyses were conducted based on treatment decisions. Results: NT-proBNP was positively correlated with CTP ischemic volume (p < 0.001), infarct core volume (p < 0.001), and ischemic penumbra volume (p < 0.001). Univariate analysis showed that the influence of NT-proBNP and functional outcomes were statistically significant in model 1 (p = 0.002). This phenomenon was persistent after adjusted for age, sex, and body mass index in model 2 (p = 0.011), adjusted for SBP, current smoking, family history of stroke, hypertension, and diabetes mellitus in model 3 (p < 0.001), and adjusted for TnI, D-dimer, PLT, Cr, TC, TG, HDL-C, treatment decisions, and NIHSS score in model 4 (p = 0.027). A high NT-proBNP was associated with a high 90-days mRS score among the total population, IV rt-PA, and standardized treatment groups, but not in IV rt-PA + EVT, EVT, and EVT/IV rt-PA + EVT groups. Conclusion: Elevated NT-proBNP levels reveal large CTP infarct core volume and poor 90-day functional outcome in AIS. NT-pro BNP is an independent risk factor for functional outcomes.

Background: Resting-state functional MRI (rs-fMRI) studies using regional homogeneity (ReHo) have identified localized functional changes in Parkinson’s disease (PD), but findings across studies exhibit considerable heterogeneity. The emerging network perspective suggests these disparate findings might reflect nodes within a single interconnected network. Functional Connectivity Network Mapping (FCNM) offers an approach to test this hypothesis.Methods: We conducted a systematic literature search (PubMed, Embase, Web of Science, CNKI, and Wanfang) for studies reporting whole-brain ReHo differences (PD vs. healthy controls). Resting-state fMRI data from the Human Connectome Project (HCP; n = 1,093) were analyzed using FCNM to map ReHo abnormalities in PD onto common functional brain networks. Robustness was assessed using 1 mm and 7 mm radii, and spatial overlap with canonical brain networks was quantified.Results: A total of 52 studies, comprising 72 datasets reporting ReHo differences between 2,052 PD patients and 1,401 healthy controls, were included in the analysis. The FCNM analysis identified a distributed PD-associated dysfunctional network. This network showed significant spatial overlap primarily with the visual (49.24%), somatomotor (32.35%), dorsal attention (44.49%), and ventral attention (67.97%) canonical networks. The network topography demonstrated high consistency across different seed radii (1 mm and 7 mm), confirming robustness.Conclusion: By integrating heterogeneous ReHo findings via FCNM, this study delineates robust PD-associated dysfunctional networks involving key sensory, motor, and attentional systems. This network-centric view offers a unifying perspective on PD pathophysiology, highlighting large-scale systems disruption and potentially reconciling previous localization inconsistencies. This approach underscores the value of network neuroscience for understanding PD mechanisms.

In order to elucidate the correlation and its pathways between liver diseases and vascular dementia (VaD). We performed two-sample Mendelian randomization (MR) study. We performed a two-sample MR study using summary-level genome-wide association study (GWAS) data for 4 liver diseases (nonalcoholic fatty liver disease [NAFLD], nonalcoholic steatohepatitis [NASH], alcoholic liver disease [ALD], and fibrosis/cirrhosis [FACOL]) and VaD. Inverse variance weighted (IVW) served as the primary analysis, complemented by a suite of sensitivity analyses (Cochran Q test, MR-Egger regression and MR pleiotropy residual sum and outlier [MR-PRESSO]). Furthermore, multivariable MR (MVMR) was conducted to adjust for key metabolic traits, including fasting glucose and triglycerides. The IVW analysis indicated that no significant causal associations were found between any of the 4 liver diseases and the risk of VaD. Sensitivity analyses indicated that the results for NAFLD and FACOL may be affected by heterogeneity, and NAFLD may also be affected by horizontal pleiotropy. Crucially, after adjusting for genetic liability to elevated triglycerides or fasting glucose in MVMR analyses, the initially null association for NAFLD became significant, revealing a protective effect against VaD. Associations for other liver diseases remained null after adjustment. This MR study found no direct causal link between liver diseases and VaD. However, adjusting for glucose or triglycerides revealed a potential protective effect of NAFLD, suggesting metabolic factors may confound the association. Further research is warranted to disentangle the complex relationship between these health conditions.

Wake-up stroke (WUS), an ischemic stroke occurring during sleep, accounts for 15-25% of acute ischemic strokes (AIS) cases and poses unique therapeutic challenges due to an unknown onset time. Circadian rhythms, regulated by the suprachiasmatic nucleus (SCN), influence various cardiovascular and metabolic processes, and disruptions of these rhythms have been implicated in stroke pathogenesis. This study explored whether WUS patients exhibit distinct circadian abnormalities compared with non-WUS patients, focusing on markers such as melatonin, cortisol, circadian clock gene expression, blood pressure (BP), and heart rate (HR). This exploratory, cross-sectional study included 28 participants (WUS: 8; non-WUS; 9, controls: 11). Blood samples were collected every 6 h over 24-h period, with melatonin and cortisol levels assessed via ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) and chemiluminescence, respectively. Circadian gene expression (CLOCK, CRY1, CRY2, PER1, PER2, and BMAL1) was analyzed using quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR). Blood pressure and HR were recorded at 2-h intervals, and circadian rhythmicity was determined using MetaCycle analysis. The results revealed significant circadian rhythms in melatonin and cortisol in the non-WUS and control groups, with WUS patients showing a complete loss of melatonin rhythm and a 3-h phase delay in cortisol. Blood pressure and HR circadian variations were absent in both stroke groups, and none of the 6 clock genes exhibited rhythmicity in either the WUS or non-WUS group. This study highlights the potential role of disrupted circadian rhythms in WUS pathogenesis, providing insights into targeted interventions such as light therapy. Future studies with larger cohorts are essential to confirm these findings and assess their clinical implications for stroke prevention and recovery.