Current Neurovascular Research - Online First

Introduction

Dizziness is one of the most common symptoms in elderly patients. In this study, we investigated changes in white matter fiber bundles in elderly patients with chronic dizziness using Automated Fiber Quantification (AFQ) to explore correlations with clinical manifestations and to provide novel insights for diagnosis.

Methods

This prospective study consecutively enrolled patients aged ≥60 years with varying degrees of white matter hyperintensities (WMH) on cranial MRI from May 2023 to October 2024. Participants were divided into a dizziness group and a non-dizziness group. Clinical data were collected for both cohorts. WMH severity and distribution were graded using the Fazekas scale, while AFQ tracked 18 cerebral white matter tracts. Between-group differences in fractional anisotropy (FA) and mean diffusivity (MD) were analyzed using independent samples t-tests.

Results

A total of 42 elderly patients were enrolled, including 24 in the dizziness group (mean age: 65.71 ± 5.46 years; 12 males, 50.0%) and 18 in the non-dizziness group (mean age: 65.56 ± 4.49 years; 7 males, 38.9%). Multivariate logistic regression revealed a significant association between deep white matter hyperintensities (DWMH) and chronic unexplained dizziness (OR = 8.285, 95% CI = 1.355–50.636, p = 0.022). AFQ demonstrated significantly reduced FA in the dizziness group within the left corticospinal tract, the greater occipital fasciculus, the left inferior fronto-occipital fasciculus, and the left arcuate fasciculus (p < 0.01). Conversely, MD was elevated in the left corticospinal tract, the large callosal clamp, the left and right inferior fronto-occipital fasciculi, the left superior longitudinal fasciculus, and the right arcuate fasciculus (p < 0.01).

Discussion

Our findings highlight that DWMH are closely linked to chronic dizziness in the elderly, and AFQ enables precise localization of microstructural damage in specific white matter tracts. These neuroimaging findings provide novel insights into the pathological mechanisms underlying chronic dizziness and offer potential imaging markers for clinical diagnosis. However, the cross-sectional design and single-center sample limit the generalization of the results, emphasizing the need for further multicenter longitudinal studies.

Conclusion

DWMH correlates with chronic dizziness in elderly patients. AFQ can identify the degree and location of white matter microstructural damage, providing new insights for clinical diagnosis and treatment.

Introduction

To delineate the distinct immunoregulatory and mitochondrial characteristics in patients with acute ischemic stroke (AIS) and intracerebral hemorrhage (ICH).

Methods

We conducted a cross-sectional study (34 AIS, 27 ICH, 30 controls) and a dynamic tracking study (1 AIS, 1 ICH). T-cell subpopulations, mitochondrial mass (MM), low mitochondrial membrane potential (MMPlow, %), and cytokine profiles were analyzed. Limitations include the small dynamic cohort and potential treatment-related confounding.

Results

The percentages of T regulatory lymphocytes (Treg%) and effector T regulatory

lymphocytes (eTreg%) were significantly higher in AIS patients than in ICH patients (p = 0.029, p = 0.017) and correlated with disease severity in AIS patients (p = 0.024, p = 0.014). The

IL-10/IL-6 ratio was significantly higher in AIS than in ICH patients (p = 0.004). AIS patients exhibited predominant changes in CD4+ (T4) lymphocyte subsets, whereas ICH patients showed more pronounced alterations in CD8+ (T8) subsets, with corresponding mitochondrial damage observed in T-cells in both groups.

Discussion

Despite limitations from the small dynamic cohort and inherent clinical confounders, this study demonstrates that AIS and ICH are characterized by distinct and evolving immune-inflammatory-mitochondrial axes. These preliminary findings highlight the role of Treg cells in AIS and suggest divergent T-cell subset involvement, providing a rationale for developing subtype-specific therapeutic strategies targeting the immune–mitochondrial axis.

Conclusion

Our study delineates a distinct immune–inflammatory–mitochondrial axis in stroke, characterized by predominant CD4+ involvement in AIS versus CD8+ T-cell alterations in ICH. These findings underscore the potential for immunomodulatory and mitochondrial-protective strategies tailored to specific stroke subtypes.

Introduction

Neuroinflammation is recognized as one of the pathogenic mechanisms underlying sepsis-associated encephalopathy (SAE). As the most commonly used anesthetic agent in the perioperative period, propofol has been demonstrated to exhibit neuroprotective and anti-inflammatory effects. This study aimed to investigate whether propofol could mitigate lipopolysaccharide (LPS)-mediated neuroinflammation and to explore the potential mechanisms.

Methods

hCMEC/D3 cells were treated with propofol, followed by LPS exposure. Western blot, ELISA, and RT-qPCR were used to assess the expression (both protein and mRNA levels) of potential pathway participants. Intracellular Fe²⁺ levels were determined using an Iron Assay Kit. In addition, an in vitro blood-brain barrier (BBB) model was constructed by co-culturing hCMEC/D3 cells and human astrocytes, and BBB permeability was assessed by measuring trans-endothelial electrical resistance (TEER).

Results

LPS (50 μg/mL, 1 h) significantly increased the secretion of TNF-α and IL-1β, induced intracellular Fe²⁺ accumulation, and upregulated the expression of 4-HNE, H3K18la, pan-Kla, and LDHA, while decreasing the expression of ZO-1, Claudin-5, and Occludin in hCMEC/D3 cells. More importantly, propofol (25 μM, 2 h) alleviated the aforementioned effects of LPS on hCMEC/D3 cells. Furthermore, we observed significant LPS-induced TEER reduction in the in vitro BBB model, and this effect was attenuated by propofol pretreatment.

Discussion

The protective effect of propofol on hCMEC/D3 cells' ferroptosis and LDHA-lactylation induced by LPS may be an important mechanism for neuroinflammation.

Conclusion

Propofol inhibits LPS-induced lactylation, ferroptosis, and release of inflammatory cytokines in hCMEC/D3 cells by downregulating the expression of LDHA.

Introduction

This study aims to identify risk factors for symptomatic intracerebral hemorrhage (ICH) in patients with old cerebral infarction.

Methods

A retrospective cohort study was conducted at Jining First People's Hospital between January 2022 and May 2024, including 287 individuals with a history of prior cerebral infarction. Study participants were classified into two groups based on the presence of symptomatic hemorrhage: those with ICH (n = 96) and those without ICH (n = 191). Logistic regression analysis was employed to identify risk factors associated with cerebral hemorrhage occurring after cerebral infarction in this population.

Results

The incidence of ICH among individuals with prior cerebral infarction was 33.48% (96/287 cases). Univariate regression analysis revealed significant differences between the ICH and the non-ICH groups in alcohol consumption, hypertension, hyperlipidemia, statin therapy, antiplatelet therapy, systolic blood pressure, diastolic blood pressure, glycosylated hemoglobin, platelet-to-lymphocyte ratio, and cerebral microbleeds (CMBs). Multivariate logistic regression analysis revealed that CMB, alcohol consumption, hyperlipidemia, and statin treatment were independent predictors of ICH in individuals with prior cerebral infarction. Additionally, CMB severity was significantly positively correlated with ICH occurrence.

Discussion

In prior cerebral infarction, CMBs, alcohol history, hyperlipidemia, and statin use independently predicted subsequent ICH, with risk escalating sharply as the CMB grade rose. These findings highlight the need to weigh aggressive lipid-lowering and antiplatelet therapy against the hemorrhagic threat signaled by CMBs and modifiable lifestyle factors.

Conclusion

The development of ICH in individuals with prior cerebral infarction is influenced by multiple factors. Effective management of CMBs, control of hyperlipidemia, alcohol abstinence, and careful adjustment of statin therapy are critical for preventing ICH. CMB severity emerges as a particularly strong predictor of ICH risk.

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