Current neurovascular research最新文献

Introduction: Current genetic research on the relationship between hypertension and vertigo is limited, and traditional observational studies cannot establish a causal relationship due to design limitations, particularly regarding whether hypertension acts as a causal risk factor for specific vertigo subtypes, such as benign paroxysmal positional vertigo (BPPV).

Methods: This study employed a two-sample MR approach to infer causal relationships via genome- wide association study (GWAS) data, thereby addressing the limitations of traditional observational studies. In addition to analyzing the link between total vertigo and hypertension, we examined three major types of vertigo: central vertigo, benign paroxysmal positional vertigo (BPPV), and other peripheral vertigo. The study included 3834 cases of BPPV, 186 cases of central vertigo, 1293 cases of other peripheral vertigo, and 209,582 controls. Various MR methods, including the inverse variance weighted (IVW) approach, MR-Egger, weighted median, and simple mode, were employed to deduce the potential causative associations.

Results: A set of 53 genome-wide significant single-nucleotide polymorphisms (SNPs) associated with hypertension was identified as instrumental variables for subsequent MR analysis. The results indicated a significantly positive correlation between hypertension and the risk of total vertigo (OR: 1.16, 95% CI: 1.08-1.25, p <0.05), BPPV (OR: 1.12, CI: 1.01-1.24, and p =0.03), and other peripheral vertigo (OR: 1.19, 95% CI: 1.00-1.41, p =0.046), whereas no significant association was found with central vertigo (OR: 1.15, 95% CI: 0.74-1.80, p =0.53).

Discussion: This study provides genetic evidence for a positive association between hypertension and vertigo, particularly BPPV and peripheral vertigo, but not central vertigo. Hypertension may induce vestibular dysfunction via vascular changes leading to tissue hypoxia and cochlearvestibular degeneration. Limitations include small sample sizes for certain vertigo subtypes (e.g., central vertigo) and limited generalizability to non-European populations.

Conclusion: This MR analysis provides evidence supporting a potential causal relationship between hypertension and an increased risk of certain types of vertigo. These findings contribute to the understanding of risk factors and the early prediction of vertigo.

Introduction: An essential component of the endocannabinoid system, cannabinoid receptor type 1 (CB1) is primarily expressed in the central nervous system, where it regulates several neurophysiological activities. Neurotransmitter release, synaptic plasticity, mood modulation, and cognitive processes are all influenced by CB1 receptors. The CB1 receptor is closely linked to a wide range of brain-related disorders, and regulating its activity may be a way to treat several brain-related diseases.

Methods: Literature search across Google Scholar, Scopus, PubMed, and Web of Science, covering publications from 1985 to 2025, aimed to gather extensive information on the pharmacological role of the CB1 receptor in various brain illnesses. Using keywords such as "CB1," "Brain," "Epilepsy," "Alzheimer's," "Parkinson's disease," "Neuroprotection," and "Neurodegeneration," this review consolidates existing knowledge and identifies potential avenues for future research.

Results: This study incorporates pre-clinical evidence and highlights the involvement of the CB1 receptor in etiologies, symptoms, and treatments related to distinct brain-related disorders.

Discussions: Potential treatment strategies that target the endocannabinoid system and the intricate relationship between CB1 receptor activity and its consequences in several brain disorders, including Parkinson's disease, Huntington's disease, Alzheimer's disease, depression, anxiety, etc., have been discussed. Additionally, the difficulties and disputes related to CB1 receptor modulation, including the contradictory actions of CB1 receptor agonists and antagonists, are also addressed.

Conclusion: The CB1 receptor is a promising therapeutic target for brain disorders due to its key role in regulating various physiological functions in the CNS, suggesting potential for the treatment of several brain disorders.

Introduction: This study aims to investigate the effect of the serum Total Cholesterol (TC) to High-Density Lipoprotein cholesterol (HDL) ratio (T/H ratio) on Hemorrhagic Transformation (HT) after Intravenous Thrombolysis (IVT) in patients with Acute Cerebral Infarction (ACI).

Methods: Patients with ACI who received alteplase were enrolled. Subgroups were classified based on the occurrence of hemorrhagic transformation (HT) after intravenous thrombolysis (IVT), whether tirofiban was coadministered, and their 90-day prognosis. The primary observation indicators were HT and the 90-day prognosis. Single-factor and multi-factor analyses were performed to identify independent predictors of HT and prognosis.

Results: Age, TC, and HDL were identified as risk factors for ACI. The T/H ratio and HDL were statistically significant in relation to HT (p < 0.05). A correlation was observed between the T/H ratio and HT, with HT more likely to occur when the T/H ratio was greater than or equal to 3.25. The use of tirofiban after IVT did not increase the risk of HT. Significant differences were observed in HT, type of HT, age, hypertension, baseline National Institutes of Health Stroke Scale (NIHSS) score, platelet volume distribution width, TC, D-dimer, and fibrinogen degradation products between groups with different prognoses.

Discussion: The T/H ratio was statistically associated with HT-ACI and predicted HT-ACI to some extent. However, the study had two limitations: the small sample size and the assessment of prognosis through follow-up phone calls, which affected the final results.

Conclusion: Patients with ACI undergoing IVT who had higher baseline NIHSS scores, lower TC, higher HDL, and a higher T/H ratio were at increased risk of HT, which was also associated with long-term outcomes. The T/H ratio may be a valuable predictor of HT following IVT.

Introduction: High On-Treatment Platelet Reactivity (HTPR) is frequently observed after carotid endarterectomy (CEA) or stenting (CAS), but its association with adverse events remains uncertain. This systematic review and meta-analysis evaluate the association between HTPR and recurrent vascular events in these patients.

Methods: EMBASE, PubMed, and Cochrane Library were searched for eligible studies from inception to July 1, 2024. Two independent reviewers screened the records, extracted data, and assessed the bias using predefined criteria. A meta-analysis was conducted using RevMan 5.4 software. The primary outcome was the risk of recurrent ischemic events in patients with HTPR. Secondary outcomes included the risk of hemorrhage and carotid restenosis.

Results: Eight studies involving 1,052 patients were included in the meta-analysis. This metaanalysis found that HTPR significantly increased the risk of adverse vascular events (OR = 2.41, 95% CI: 1.37-4.24), particularly in CAS patients (OR = 1.85, 95% CI: 1.14-2.98), but not in CEA patients (OR = 4.53, 95% CI: 0.52-39.12). Furthermore, HTPR was not significantly associated with an increased risk of bleeding (OR = 0.90, 95% CI: 0.24-3.37) or carotid restenosis (OR = 1.70, 95% CI: 0.38-7.55).

Discussion: This meta-analysis demonstrates that HTPR may increase the risk of recurrent ischemic events in CAS patients, supporting the clinical utility of platelet function monitoring in this population. However, no significant association was observed between HTPR and hemorrhage or restenosis. These findings should be interpreted cautiously due to study limitations, including small sample sizes and heterogeneity in platelet function assessment methodologies. Large-scale prospective studies with standardized protocols are warranted to validate these observations.

Conclusion: HTPR may be associated with an increased risk of recurrent ischemic events in patients undergoing CAS, highlighting the potential value of platelet function monitoring.

Background: With 301 million cases worldwide, anxiety disorders represent a serious public health concern. Many people endure ongoing distress while receiving several treatments because of the drawbacks of traditional therapy, such as adverse effects, dependence, and inconsistent efficacy. This emphasizes the absolute need for novel treatment approaches.

Objective: This review examines emerging pharmacological and non-pharmacological strategies for anxiety disorders, assessing existing and developing therapeutic options while examining the drawbacks of conventional therapies.

Methods: A comprehensive literature review was carried out using the NIH, PubMed, and Google Scholar databases. Studies from 2020-2025 were given priority in the inclusion criteria, with a few supporting references from earlier years. Personalized medicine, combination therapy, non-pharmacological interventions, and novel anxiolytic targets, etc., were among the keywords used.

Results: Conventional therapies, including benzodiazepines, SSRIs, and SNRIs, are still the major choices, but they have significant disadvantages. The protein kinase pathway, endocannabinoid and orexin systems, NK1R antagonists, and microbiome modulation are examples of emerging targets. Emerging strategies that show preliminary promise include digital therapeutics, gene therapy, optogenetics, personalized medicine, combination therapy, herbal therapy, and peptide-based medicines (e.g., NPY, NPS, oxytocin analogs, CRF, vasopressin, and melanocortin receptor antagonist). Several of these approaches modulate key neural circuits, such as the involvement of the amygdala-prefrontal cortex axis, via the HPA axis, and biomarker-informed personalization, among others; yet many remain in early-phase or preclinical investigation. However, limited comparative data exist between these novel strategies and standard therapies, underlining the need for rigorous head-to-head evaluations.

Conclusion: Advances in molecular neuroscience and precision medicine offer potential alternatives to conventional treatments. However, most emerging therapies require further clinical validation, large-scale trials, and translational refinement before they can be integrated into realworld decision-making for anxiety disorders.

Introduction: Post-stroke dysphagia (PSD) is a common complication after acute stroke. It can be effectively alleviated by electroacupuncture (EA) stimulation at the Baihui acupoint; however, the underlying mechanism remains unclear.

Methods: Male ICR mice were used, and the suture occlusion method was employed to establish the middle cerebral artery occlusion (MCAO) mouse model. EA stimulation was applied to the Baihui acupoint for intervention. After treatment, the survival rate of the mice was assessed. Subsequently, a water swallow test was conducted to evaluate the degree of dysphagia in the mice. Additionally, neurological function was assessed through Garcia scoring and measurement of serum Ca2+-Mg2+-ATPase activity. Fur-thermore, MRI was utilized to evaluate the therapeutic effects of EA on cerebral infarction and edema rates. Then, the antioxidant activity of the EA intervention was assessed by measuring indicators of oxida-tive damage. Finally, the expressions of gamma- aminobutyric acid type B receptor subunit 1 (GAB-ABR1), N-methyl-D-aspartate receptor 1 (NMDAR1) were detected through WB, RT-qPCR, and immu-nofluorescence.

Results: EA intervention effectively increased the survival rate of MCAO mice and alleviated their dysphagia. Additionally, the impaired neurological function of the mice was improved, and cerebral infarction and edema rates were reduced. Furthermore, EA alleviated oxidative stress in mice, reduced damage to neurons in the nucleus ambiguus, and upregulated GABABR1 while downregulating NMDAR1.

Discussion: Although we suggested that EA may exert therapeutic activity for PSD by maintaining the balance of NMDAR1 and GABABR1, this conclusion still requires further experimental validation.

Conclusion: EA stimulation of the Baihui acupoint was effective in treating PSD, which was related to its ability to improve damaged neurons, upregulate GABABR1, and downregulate NMDAR1. These findings provided a new insight into the mechanisms of EA treatment for PSD and serve as a theoretical basis for future clinical research.

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Background: Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury.

Methods: The Oxygen-Glucose Deprivation/Re-oxygenation (OGD/R) model was employed in primary mouse astrocytes, and the Middle Cerebral Artery Occlusion (MCAO) model was established in mice to mimic ischemia-reperfusion-induced injury. Si-circ0001679, anti-miR- 216, and TLR4 ORF-clone were transfected either in cells or mice to study the molecular mechanisms during I/R-induced injury. Inflammation and oxidative stress were monitored after treatment.

Results: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress.

Conclusion: This study unveiled a novel regulatory axis of circ0001679-miR-216-TLR4 in I/Rinduced brain injury. Targeting circ0001679 may represent a promising therapeutic strategy for I/R-induced brain injury.