Resveratrol (RES), a naturally occurring polyphenolic compound found in grapes, berries, and peanuts, has attracted considerable interest because of its antioxidant, anti-inflammatory, and neuroprotective properties. This narrative review examines the current evidence regarding the potential effects of RES on memory-related processes and neuroinflammatory biomarkers in major neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and cerebral ischemia. Relevant literature was identified through searches of major scientific databases, and studies addressing the molecular mechanisms, experimental outcomes, and therapeutic implications of RES in these conditions were evaluated. The available evidence indicates that RES can modulate several biological pathways associated with neurodegeneration, including oxidative stress, inflammatory signaling, mitochondrial dysfunction, and neuronal survival. Experimental studies suggest that RES may influence key molecular mediators such as pro-inflammatory cytokines, nitric oxide (NO) signaling, and matrix metalloproteinases, which are implicated in neuronal damage and blood-brain barrier disruption. In preclinical models of AD and PD, RES has been associated with improvements in cognitive performance, reduction of neuroinflammatory markers, and attenuation of neuronal loss. Similarly, studies in MS and cerebral ischemia models indicate that RES may modulate immune responses, reduce oxidative damage, and limit ischemia-related neuronal injury. However, most of the current evidence derives from in vitro and animal studies, and clinical data remain limited. Moreover, the low bioavailability of RES and variability in dosing regimens represent important challenges for clinical translation. Therefore, although experimental findings support the potential neuroprotective role of RES, further well-designed clinical studies are required to determine its therapeutic relevance and safety in human neurological disorders. This narrative review was developed through a structured search of PubMed, Scopus, and Web of Science for articles published between 2000 and 2024, focusing on mechanistic, preclinical, and clinical investigations of RES in neurological disorders. This review synthesizes current evidence on the molecular and cellular mechanisms underlying the neuroprotective effects of RES, with particular emphasis on its antioxidant, anti-inflammatory, and immunomodulatory activities. By integrating findings from experimental and clinical research, the review highlights the potential of RES to modulate key pathways involved in neurodegeneration and neuroinflammation. Although further well-designed clinical studies are required to clarify its therapeutic efficacy and translational relevance, the available evidence supports continued investigation of RES as a promising candidate for neuroprotective strategies in neurological disorders.

Carotid bifurcation geometry influences local hemodynamics and may contribute to plaque formation and carotid disease. Interethnic differences in carotid bulb geometry remain incompletely characterized. However, Asian populations are known to have less atherosclerosis burden in the extracranial carotid arteries compared to White populations.

In a cross-sectional study (2022-2025), 200 adults without relevant carotid stenosis were enrolled consecutively (100 White participants in Germany; 100 Asian participants in China). Carotid geometry was assessed bilaterally using predefined diameter ratios; Carotid bulb (CB)/Internal carotid artery (ICA) diameter was the prespecified primary outcome. Linear mixed-effects models accounted for within-subject correlation; adjusted models included age, sex, BMI, diabetes, hypertension, dyslipidemia, smoking, and atrial fibrillation.

In unadjusted models, significant ethnic differences were observed across all primary geometry ratios. CB/ICA was lower in Asian versus White participants (EMM 1.57 vs. 1.68; p < 0.001). After adjustment, the CB/ICA difference remained robust (Asian minus White -0.09; 95% CI -0.14 to -0.04; p < 0.001). Additional adjusted differences were observed for CB/CCA, ICA/CCA, ECA/ICA, and outflow/inflow, whereas no significant difference persisted for ECA/CCA. Analyses of absolute diameters showed no significant interethnic difference in ICA diameter, while carotid bulb diameter was smaller in Asian participants.

Carotid bifurcation geometry differs between Asian and White adults independent of vascular risk factors. These anatomical differences may have implications for carotid hemodynamics and plaque formation across populations.

Intracerebral hemorrhage (ICH) is commonly encountered in elderly patients. Peroxiredoxin 6 (Prx6) is involved in oxidative stress and inflammatory responses. Here, serum Prx6 levels were measured to explore their prognostic value in ICH.

In this multicenter observational analytical study of 306 elderly patients with ICH and 100 elderly controls, serum Prx6 levels were quantified at admission of all patients, at serial time points of 103 patients and at study entry of controls. Outcome variables included early neurological deterioration (END) and poor neurological status mirrored by six-month modified Rankin Scale (mRS).

Serum Prx6 levels were significantly elevated upon admission of patients, gradually increased on day 1, peaked on day 3, decreased from day 5 until day 14 after ICH, and were markedly higher during 14 days than those of controls. Serum Prx6 levels, in independent correlation with National Institutes of Health Stroke Scale scores, hematoma sizes and mRS scores, were linearly related to risks of END and poor prognosis, and independently predicted their occurrences. The independent associations were robust in sensitivity analysis. The association between serum Prx6 levels and poor prognosis was partially mediated by END. Serum Prx6 levels showed an effective predictive ability for poor prognosis and END. Other parameters, such as age, gender, and hypertension, negligibly affected the relevance of Prx6 levels in poor prognosis and END. The combined models encompassing independent predictors were visualized via the nomograms and had acceptable goodness of fit and clinical benefit via various statistical tools.

Elevated serum Prx6 levels post-ICH in the elderly are intimately related to bleeding severity and clinical outcomes; and END partially interprets the association of serum Prx6 with poor prognosis, therefore suggesting that serum Prx6 may be a prognostic biomarker of ICH in the elderly.

The prevalence of polypharmacy has been rising worldwide, most studies focuses on older adults. However, little is known about patterns and determinants of polypharmacy in middle-aged individuals engaged in structured national prevention programmes. This exploratory study examines how clinical characteristics, comorbidity structure, and system-level actions relate to increasing medication burden in participants of the Polish Prophylaxis 40 PLUS prevention programme, which focuses on the prevention and early detection of lifestyle-related (civilization) diseases, particularly cardiovascular conditions.

A cohort of 151 adults aged ≥40 years was stratified into three ordinal polypharmacy categories (5, 6, ≥7 drugs). Patients demographics, lifestyle behaviours, blood-pressure measures, ICD-10 comorbidity blocks, and indicators of medical actions were analysed. Ordinal proportional-odds regression (forward and backward stepwise selection) was performed with multimorbidity included as an adjustment covariate. Bootstrap resampling (B = 200) assessed parameter stability.

Circulatory system diseases (ICD-10 I) were consistently associated with higher odds of belonging to a higher polypharmacy category (OR 2.3-2.6). Normalisation of previously irregular heart rhythm strongly predicted higher medication burden (OR 6.0-8.4). Sensory system diseases (ICD-10 H) were also positively associated with polypharmacy, whereas nervous-system diseases (ICD-10 G) showed an inverse relationship. Higher baseline diastolic blood pressure was negatively associated with medication count (OR 0.93-0.95 per mmHg). Educational attainment demonstrated a weaker, exploratory positive association. Bootstrap analysis confirmed the robustness of the main predictors (ICD-10 I, ICD-10 G/H, heart-rhythm change, baseline DBP).

In middle-aged adults within a Polish national prevention programme, polypharmacy reflects treatment intensity and system-level complexity rather than multimorbidity alone. Cardiovascular disease, rhythm-control interventions, and multi-specialty care were associated with higher medication burden. These findings highlight the importance of integrating structured medication review, targeted deprescribing, and equitable preventive pharmacotherapy into cardiovascular prevention pathways.

Impaired endogenous vascular regenerative capacity, reflected by reduced circulating progenitor cell (CPC) counts, has been linked to age-related diseases, particularly adverse cardiovascular outcomes. Lower CPC counts have also been associated with accelerated age-related cognitive decline in otherwise healthy individuals, but their relationships with cognitive impairment and neuroimaging markers of vascular brain injury and neurodegeneration remain unclear. We investigated cross-sectional associations between CPC subsets, cognitive performance, and neuroimaging phenotypes, hypothesizing that lower CPC levels would be associated with worse cognition and adverse brain markers.

In 283 community-dwelling participants (mean age, 65 years; 59% female, 39% Black) enrolled in the Brain Stress, Hemodynamics and Risk Prediction program, cognitive assessments (including Montreal Cognitive Assessment), brain magnetic resonance imaging-derived white matter hyperintensity volumes, and whole-brain cortical thickness were measured. Flow cytometry is used to enumerate CPCs as CD45^med mononuclear cells expressing CD34 with coexpression of either CD133, chemokine CXCR4 (CXC motif receptor 4), or VEGFR2⁺ (vascular endothelial growth factor receptor-2). Linear regression models were adjusted for demographic and vascular risk factors.

In fully adjusted models, lower CD34⁺/CD133⁺ CPC levels were associated with worse global cognition (Montreal Cognitive Assessment: β=0.59; P=0.01), lower mean cortical thickness (β=0.01; P=0.01), and greater white matter hyperintensity burden (β=-0.15; P=0.01). Similarly, lower CD34⁺ and lower CD34⁺/CXCR4⁺ CPC levels were significantly associated with greater white matter hyperintensity volume (CD34⁺: β=-0.27, P<0.01; CD34⁺/CXCR4+: β=-0.14, P=0.03). CD34⁺/VEGFR2⁺ CPC levels were associated with Montreal Cognitive Assessment (β=0.37, P<0.01) and Boston Naming Test performance (β=0.01, P=0.03), but not with neuroimaging phenotypes.

Reduced regenerative capacity was associated with worse global cognitive performance and markers of vascular brain injury, including greater white matter hyperintensity burden and cortical thinning. These findings should be validated in longitudinal studies to clarify temporality and potential causality.

Vascular Ehlers-Danlos syndrome (vEDS) is a life-threatening connective tissue disorder that often remains undiagnosed before pregnancy and carries a markedly high risk of maternal mortality. We report the case of a 34-year-old pregnant woman who experienced sudden abdominal pain at 39 weeks of gestation and died shortly after delivery. Autopsy revealed an aortic rupture with histopathological findings suggestive of vEDS. Her family history included her father's sudden vascular death, and her personal history was notable for easy bruising and early-onset varicose veins. Next-generation sequencing-based postmortem genetic testing (PMGT) using formalin-fixed, paraffin-embedded liver tissue confirmed a pathogenic variant in COL3A1. This result facilitated genetic counseling for the family, allowing presymptomatic diagnosis and preventive management, including celiprolol therapy for at-risk relatives. This case underscores the value of PMGT in identifying the underlying cause of unexpected maternal death, particularly when conventional samples are unavailable.

The heartbeat evoked potential (HEP) is an electrophysiological indicator of cortical processing of cardiac signals and a putative neural index of cardiac interoception. Various clinical conditions are associated with disrupted heart-brain communication, raising the possibility that the HEP could serve as a valid biomarker of disrupted cardiac interoception. Yet there is limited understanding about how the HEP signal, and its various parameters, is associated with different health conditions.

We synthesised the current evidence for HEP amplitude as a biomarker across all available clinical subpopulations using a random-effects multilevel meta-analysis. Secondly, we systematically characterised and quantitatively evaluated key HEP parameters, such as latency windows, reference electrodes, and scalp topographies across HEP studies (OSF Doi: 10.17605/OSF.IO/TMQ3W).

Subgroup analyses for each condition showed no difference in HEP amplitude between clinical conditions relative to healthy comparisons; however, large negative effect estimates were found in neurological and cardiovascular diseases, though these were based on a small number of studies and should be interpreted with caution. In subsequent multivariate analysis, clinical category partially explained the global variability in HEP parameters.

Based on these results, no firm conclusions can be drawn regarding the utility of HEP amplitude as a clinical biomarker. Substantial heterogeneity and widespread methodological inconsistencies across studies preclude definitive interpretations, and rigorous, standardised research is needed before the clinical value of HEP can be established.

High blood pressure in children is rare and often underdiagnosed, but it can cause irreversible damage to target organs. Ocular signs of hypertensive retinopathy are nonspecific and may resemble those of neuroretinitis or papilledema, which can delay diagnosis.

A 9-year-old girl presenting with bilateral visual loss was referred to our emergency department. Best-corrected visual acuity was 20/200 in the right eye and counting fingers in the left. Fundus examination revealed bilateral optic disc swelling with a macular star and flame-shaped hemorrhages. Infectious work-up and neuroimaging were inconclusive. Reassessment showed severe hypertension (165/118 mmHg), hypokalemia, impaired renal and cardiac function. Plasma renin and aldosterone were markedly elevated. Imaging revealed a hypoplastic left kidney with subtotal renal artery stenosis and high-grade vesicoureteral reflux, contributing only 7% of total renal function on DMSA scintigraphy. Antihypertensive therapy with amlodipine, enalapril, and acebutolol normalized blood pressure, improved renal and cardiac function, and restored full visual acuity within six months. A left nephrectomy was subsequently performed to improve long-term blood pressure control.

This case demonstrates the importance of systematic blood pressure measurement in children with disc edema or neuroretinitis-like features. Severe hypertension should be considered early on. Pediatric guidelines recommend blood pressure targets below the 90th percentile with ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, or thiazide diuretics as first-line agents. Nephrectomy may be indicated in cases of refractory hypertension when a hypoplastic kidney contributes less than 10% of overall function.

Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute myocardial infarction (MI), particularly among young to middle-aged women without traditional cardiovascular risk factors. This review summarizes recent advances in the understanding, diagnosis, and management of SCAD.

SCAD results from an intramural hematoma (IMH) or intimal tear causing separation of the coronary arterial wall and compression of the true lumen. Fibromuscular dysplasia is the most consistently associated arteriopathy, supporting a systemic vascular vulnerability. Genetic studies suggest a predominantly polygenic architecture, with variants such as PHACTR1 implicated in vascular signaling and endothelial regulation. Coronary angiography remains the diagnostic cornerstone, with intracoronary imaging aiding in uncertain cases, while emerging non-invasive modalities such as photon-counting computed tomography may refine non-invasive diagnosis. Conservative management is preferred in most stable patients because spontaneous healing is common and percutaneous coronary intervention carries procedural challenges. Persistent angina, coronary vasospasm, microvascular dysfunction, and psychological distress are increasingly recognized components of recovery. Multidisciplinary follow-up incorporating cardiac rehabilitation and psychological support is essential to address persistent symptoms and recovery after SCAD. SCAD is a distinct non-atherosclerotic cause of MI driven by an underlying arteriopathy and systemic vascular vulnerability, requiring individualized management, vascular screening, and multidisciplinary follow-up. Ongoing randomized trials and genomic studies aim to refine risk stratification, clarify optimal medication strategies, and improve long-term outcomes and recurrences.

This study examines the short-term associations and potential long-term causal effects of environmental temperature and air pollution exposures on the risk of acute Stanford Type A Aortic Dissection (AAAD). We conducted a time-series analysis in Shenyang, Northeast China, using daily meteorological and air quality data matched with hospital admissions for AAAD from Shengjing Hospital of China Medical University. Daily mean temperature ranged from approximately - 20 °C to 20 °C, while PM_2.5 concentrations exhibited episodic spikes up to 600 µg/m³. A distributed lag non-linear model (DLNM) evaluated lagged exposure - response relationships over a 28-day period. The DLNM revealed a pronounced inverse J-shaped relationship between mean temperature and AAAD risk: exposure to cold temperatures below 0 °C was associated with a significantly elevated relative risk (RR), with persistent effects noted from lag 5 to lag 20 days. PM_2.5 exhibited a U-shaped association with AAAD, with the highest risks observed at concentrations near 250 µg/m³ within 0-4 days post-exposure. Joint exposure surfaces demonstrated complex interplay between cold and particulate matter on AAAD incidence. To explore potential long-term causal effects, we performed two-sample Mendelian randomization analyses using genetic instruments for workplace temperature conditions and for chronic exposure to air pollutants (PM_2.5, PM₁₀ and NO₂). The primary inverse-variance weighted analysis showed non-significant associations for genetically instrumented "often cold" workplace exposure (e.g., OR = 0.23; 95% CI: 0.0004-142.62; P = 0.655) and likewise provided no robust evidence for causal effects of long-term PM2.5, PM₁₀ or NO₂ exposure on AAAD risk, with wide confidence intervals encompassing the null. These findings highlight significant short-term associations of cold and high pollution exposures with AAAD incidence, whereas long-term causal links inferred from genetic proxies for workplace temperature and air pollutants remain unconfirmed and require further investigation.