The International Journal Of Neuroscience[JOURNAL]
Sun
200 papers
The correlation between gene polymorphism and cognitive dysfunction after radiotherapy for glioma.
Zhu H, Shi X, Zong D … +1 more , He X
Int J Neurosci · 2026 Jun · PMID 41689464 · Publisher ↗
BACKGROUND: Gliomas are the most common primary malignant tumors of the central nervous system. Mounting evidence highlights the crucial role of YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) in glioma treatment r...
BACKGROUND: Gliomas are the most common primary malignant tumors of the central nervous system. Mounting evidence highlights the crucial role of YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) in glioma treatment response. This study aimed to investigate the association between single-nucleotide polymorphisms (SNPs) of YTHDF1 and cognitive dysfunction (CD) following radiotherapy for glioma. METHODS: A total of 323 glioma patients were enrolled pre-radiotherapy and followed up for 3 months post-radiotherapy. They were categorized into glioma patients with CD (group, = 202) and glioma patients without CD (non-CD group, = 121). YTHDF1 mRNA expression was measured in peripheral blood samples collected before radiotherapy using RT-qPCR. Four YTHDF1 SNPs (rs6011668, rs6090311, rs68041888 and rs6122103) were genotyped PCR-RFLP. Multivariate logistic regression was further performed to verify the association between YTHDF1 polymorphisms and post-radiotherapy CD. RESULTS: YTHDF1 mRNA expression was significantly higher in the CD group than in the non-CD group. Among the four analyzed SNPs, only rs6090311 exhibited significant differences in both genotype and allele frequencies between the two groups, while rs6011668, rs68041888 and rs6122103 showed no significant variations. After controlling for potential confounders, including WHO grade, tumor volume, BDNF levels, and radiotherapy dose, carriers of the G allele (A/G + G/G genotypes) at rs6090311 demonstrated a significantly lower risk of developing post-radiotherapy CD (OR = 0.319, 95% CI: 0.111-0.916). CONCLUSIONS: YTHDF1 overexpression is associated with post-radiotherapy CD in glioma patients, and the rs6090311 G allele may act as a protective genetic marker for this complication.
Deep learning-based epileptic seizure detection from EEG signals and PPG signals using LSTM and CNN models.
B AD
Int J Neurosci · 2026 May · PMID 41671683 · Publisher ↗
Epilepsy is a chronic neurological disorder characterized by recurrent and unpredictable seizures that significantly affect patients' health and quality of life. Conventional diagnosis relies heavily on continuous electr...
Epilepsy is a chronic neurological disorder characterized by recurrent and unpredictable seizures that significantly affect patients' health and quality of life. Conventional diagnosis relies heavily on continuous electroencephalogram (EEG) monitoring, which requires clinical expertise and is not well suited for real-time detection. To address these challenges, this article presents a hybrid deep learning framework that integrates convolutional neural networks (CNNs) and long short-term memory (LSTM) models for automated epileptic seizure (ESD) detection using multimodal EEG and Photoplethysmogram (PPG) signals. Unlike EEG-only approaches, the inclusion of PPG provides complementary physiological information, such as autonomic fluctuations, seizure-induced heart rate variability (HRV) changes and peripheral vascular responses - which strengthens the model's discriminative capability, particularly in cases where EEG signatures alone are subtle or ambiguous. In the proposed framework, CNNs effectively extract spatial patterns from the preprocessed biosignals, while LSTMs capture temporal dependencies associated with seizure evolution. Data preprocessing steps including filtering, normalization, segmentation and augmentation are applied to enhance signal quality and model generalization. The hybrid CNN-LSTM model is evaluated on benchmark EEG-PPG datasets using accuracy, precision, recall, F1-score, Cohen's Kappa, Matthews Correlation Coefficient (MCC) and Critical Success Index (CSI). Comparative analysis with existing state-of-the-art models demonstrates superior performance and robustness. Overall, the proposed multimodal deep learning system offers a reliable and efficient solution for real-time seizure detection, with strong potential for deployment in wearable and clinical healthcare platforms.
Evaluating the efficacy and safety of Edaravone-Dexborneol in acute ischemic stroke: an updated systematic review and meta-analysis of 7,846 Chinese patients.
Sabet H, Abbas A, Zanaty MA … +6 more , Elyamany Z, El-Moslemani M, Pereira MAOM, Al-Mufti J, Abdelnaby R, Elfil M
Int J Neurosci · 2026 Jun · PMID 41655025 · Publisher ↗
OBJECTIVE: To evaluate the safety and efficacy of Edaravone-Dexborneol (EDB) as a neuroprotective agent in patients with acute ischemic stroke (AIS). METHODS: We conducted a comprehensive search in PubMed, Scopus, Web of...
OBJECTIVE: To evaluate the safety and efficacy of Edaravone-Dexborneol (EDB) as a neuroprotective agent in patients with acute ischemic stroke (AIS). METHODS: We conducted a comprehensive search in PubMed, Scopus, Web of Science, and Cochrane CENTRAL until January 22, 2026, including clinical trials and observational studies comparing EDB with edaravone monotherapy, standard treatment, and placebo. Data on functional recovery (Modified Rankin Scale [mRS], National Institutes of Health Stroke Scale [NIHSS], Barthel Index [BI]), safety outcomes, and mortality were extracted. A random effects model was used for statistical analysis. RESULTS: Overall, 13 studies (5 cohort studies and 8 randomized controlled trials) involving 7,846 patients were included, demonstrating that EDB significantly improved 90-day mRS scores (0-1) compared with edaravone alone (RD: 0.08, 95% CI: [0.03, 0.13], = 0.001). When compared with standard treatment, NIHSS scores were significantly lower in the EDB group (MD: -2.18, 95% CI: [-3.75, -0.62], = 0.006), and no significant difference was observed in mRS (0-1) or the risk of symptomatic intracranial hemorrhage (sICH). Safety outcomes showed a possible dose-dependent adverse event (AE), including hyperhomocysteinemia and hypokalemia. CONCLUSION: EDB might be an effective treatment for improving functional recovery in patients with AIS and appears to have a relatively favorable safety profile. However, careful dosing is necessary to minimize AEs. Future research should focus on large-scale trials, long-term outcomes, and mechanistic studies to optimize treatment protocols.
A predictive model for postoperative delirium in patients admitted to the intensive care unit after cardiac valve surgery.
Shi Z, Yuan Z, Cheng J … +1 more , Zhao Y
Int J Neurosci · 2026 May · PMID 41652661 · Publisher ↗
INTRODUCTION: Postoperative delirium (POD) frequently occurs in patients following cardiac valve surgery in the intensive care unit (ICU), and is linked to adverse outcomes and extended hospitalization. The purpose of th...
INTRODUCTION: Postoperative delirium (POD) frequently occurs in patients following cardiac valve surgery in the intensive care unit (ICU), and is linked to adverse outcomes and extended hospitalization. The purpose of this study was to establish and validate a model for predicting high-risk individuals. METHODS: This retrospective analysis enrolled adult patients who had cardiac valve surgery and subsequent ICU admission. Potential predictors were screened using LASSO logistic regression with cross-validation, followed by multivariable logistic regression, and a nomogram was developed from the final model. Model performance was assessed by receiver operating characteristic (ROC) curve analysis, calibration plots and decision curve analysis (DCA), and was benchmarked against the Sequential Organ Failure Assessment (SOFA) score. RESULTS: In total, 3249 patients were analyzed, of whom 535 (16.5%) developed POD. Significant predictors identified were oxygen saturation, respiratory rate, urea nitrogen, INR, white blood cell (WBC) count, hemoglobin, SOFA score, myocardial infarction, diabetes and hyperlipidemia. The nomogram yielded AUCs of 0.766 (95% CI: 0.738-0.794) in the training cohort and 0.789 (95% CI: 0.750-0.828) in the validation cohort, showing significantly better predictive accuracy than the SOFA score ( < 0.05). CONCLUSIONS: The proposed model demonstrates strong predictive ability for POD in cardiac valve surgery patients and may aid clinicians in early risk stratification and targeted intervention. Further prospective validation is needed.
Time-dependent neurovascular unit dysfunction in ischemic stroke: mechanisms of neurovascular uncoupling and its clinical impact.
Lahariya R, Sinha M, Kumari B … +2 more , Subramanian KV, Anand G
Int J Neurosci · 2026 Jun · PMID 41642667 · Publisher ↗
AIM: Neurovascular unit (NVU) dysfunction is a central determinant of tissue injury, reperfusion failure, and long-term neurological outcomes after ischemic stroke. This review critically examines the cellular and molecu...
AIM: Neurovascular unit (NVU) dysfunction is a central determinant of tissue injury, reperfusion failure, and long-term neurological outcomes after ischemic stroke. This review critically examines the cellular and molecular mechanisms underlying NVU disruption, with a particular focus on inflammation, oxidative stress and blood-brain barrier (BBB) integrity, and evaluates emerging NVU-targeted therapeutic strategies. METHODS: A focused narrative review synthesized studies on ischemic stroke-related NVU alterations, integrating cellular mechanisms, biomarkers and phase-specific therapeutic strategies targeting BBB dysfunction, inflammation, oxidative stress and neurorestoration. RESULTS: Acute ischemic injury induces endothelial tight-junction disruption, pericyte constriction and loss, astrocytic activation and microglial-driven inflammation, resulting in BBB breakdown, impaired neurovascular coupling (NVC) and restricted microvascular reperfusion. These processes facilitate leukocyte infiltration, exacerbate secondary neuronal damage and increase hemorrhagic transformation risk. Circulating and cerebrospinal fluid (CSF) biomarkers, including MMP-9, GFAP, S100B and pro-inflammatory cytokines, reflect NVU injury severity and correlate with functional outcomes. In the chronic phase, persistent BBB permeability, maladaptive VEGF signaling and sustained low-grade inflammation contribute to white matter injury, impaired neuroplasticity and post-stroke cognitive decline. Therapeutic strategies targeting NVU dysfunction include anti-inflammatory agents, COX-2 inhibitors and NADPH oxidase (NOX) inhibitors, alongside stem cell-based and extracellular vesicle-mediated approaches that promote vascular stabilization and repair. Neuroplasticity-enhancing interventions and nanoparticle-based drug delivery systems further support functional recovery. CONCLUSIONS: NVU dysfunction underlies both acute injury amplification and chronic recovery failure after stroke. Biomarker-guided, phase-specific therapeutic strategies targeting inflammation, oxidative stress and BBB instability represent a promising framework for personalized stroke management.
Genetically predicted artificial sweeteners and stroke susceptibility: a multivariable Mendelian randomization study.
Song Z, Li H, Zhang Y
Int J Neurosci · 2026 Jun · PMID 41640371 · Publisher ↗
AIMS: The present study investigated the causal associations of artificial sweetener consumption on the risk of stroke. METHODS: We applied a two-sample Mendelian randomization (MR) design using genome-wide association s...
AIMS: The present study investigated the causal associations of artificial sweetener consumption on the risk of stroke. METHODS: We applied a two-sample Mendelian randomization (MR) design using genome-wide association study (GWAS) summary data for artificial sweetener intake (added to coffee, tea, and cereal) and stroke. The primary inverse variance weighted (IVW) analysis was complemented by sensitivity tests (Cochran's Q-test, MR-Egger, MR-PRESSO, and leave-one-out analysis) and multivariate MR (MVMR) to address heterogeneity, pleiotropy, and potential confounding. RESULTS: Artificial sweeteners added to tea nominally increased small vessel stroke risk (OR = 3.01, 95%CI: 1.28-7.07, = 0.0115, P-FDR = 0.20). Low-calorie drink intake (OR = 1.71, 95%CI: 1.12-2.63, = 0.014, P-FDR = 0.20) and sucralose metabolite levels (OR = 1.14, 95%CI: 1.02-1.27, = 0.029, P-FDR = 0.20) were nominally associated with cardioembolic stroke. MVMR analysis revealed that after adjusting for coffee intake, the association between intake of artificial sweeteners added to tea and small vessel stroke (OR = 2.90, = 0.024) remained statistically significant. And after adjusting for blood glucose levels, the association between sucralose metabolite levels and cardioembolic stroke reversed direction and remained statistically significant (OR = 0.73, = 0.024). CONCLUSION: This MR study indicated that artificial sweeteners, particularly those added to tea and sucralose metabolites, were associated with small vessel and cardioembolic stroke, respectively. However, these associations were attenuated after adjusting for BMI or tea consumption, indicating potential confounding by adiposity or beverage habits. Findings should be interpreted cautiously and warrant further investigation.
A systems biology framework uncovers multi-level genetic regulation of dizziness/vertigo through eQTL-GWAS integration and single-cell analysis.
Shan D, Li S, Zhang L … +2 more , Bai J, Wang H
Int J Neurosci · 2026 Jun · PMID 41640369 · Publisher ↗
BACKGROUND: Dizziness/vertigo is a multifactorial neurological disorder with complex ge-netic and cellular bases, yet its molecular mechanisms remain unclear. Understanding how gene regulation contributes to dizziness/ve...
BACKGROUND: Dizziness/vertigo is a multifactorial neurological disorder with complex ge-netic and cellular bases, yet its molecular mechanisms remain unclear. Understanding how gene regulation contributes to dizziness/vertigo may reveal novel neurobiological and therapeutic insights. METHODS: We established a multi-omics integrative framework combining genome-wide association study (GWAS) data with expression quantitative trait loci (eQTL) from brain single-cell types, CD4 T cells, oneK1K immune cells, and plasma. Two-sample Mendelian randomization (MR) and colocalization analyses were applied to identify causal genes. Single-cell RNA sequencing (scRNA-seq) of the auditory nerve was used to as-sess cell type-specific expression, intercellular communication, and pseudotime dynam-ics. Gene-gene interaction and drug-target networks were further constructed to identify potential therapeutic candidates. RESULTS: Six key genes-Activin A Receptor Type 2 A (), Phospholipid Transfer Protein (), Androgen Dependent TFPI Regulating Protein (), Methylenetetrahydrofolate Dehydrogenase (NADP+ Dependent) 1 Like (), Collagen Type VII Alpha 1 Chain (), and Pantothenate Kinase 4 ()-showed strong causal and colocalization evidence for dizziness/vertigo. Single-cell analysis revealed distinct cell type-specific expression, with fibroblasts and adipocytes playing central roles in signaling and gene regulation. Pseudo-time trajectories indicated coordinated upregulation of , , , and during later developmental stages. Interaction network analysis positioned these genes as major hubs, and DrugBank screening identified Sotatercept as a promising candidate targeting . CONCLUSION: This integrative analysis links gene expres-sion regulation to dizziness/vertigo across neuroimmune and metabolic systems. The findings uncover coordinated molecular pathways underlying disease susceptibility and highlight novel therapeutic targets, providing a foundation for precision treatment strate-gies.
Effects of alteplase, aspirin, and clopidogrel on inflammatory factors and neurological function in patients with stroke.
Chen J, Yang X, Zhao Z
Int J Neurosci · 2026 Jun · PMID 41636554 · Publisher ↗
AIM: To evaluate the clinical value of combining alteplase, aspirin, and clopidogrel in patients with stroke, with changes in the National Institutes of Health Stroke Scale (NIHSS) score as the primary efficacy assessmen...
AIM: To evaluate the clinical value of combining alteplase, aspirin, and clopidogrel in patients with stroke, with changes in the National Institutes of Health Stroke Scale (NIHSS) score as the primary efficacy assessment indicator. METHODS: Clinical data of 122 patients with stroke who received pharmacological treatment between January 2022 and June 2024 were retrospectively collected from the hospital's health information technology (HIT) system. Patients were assigned to two groups according to treatment protocols: a dual-agent group ( = 61; aspirin plus alteplase) and a triple-agent group ( = 61; alteplase, aspirin, and clopidogrel). RESULTS: At 24 h, 3 days, and 5 days of treatment, NIHSS scores were lower in the triple-agent group than in the dual-agent group, with a significantly higher NIHSS improvement rate at 5 days (85.0% vs. 75.0%, = 0.022). At 5 days and at 90-day follow-up, Montreal Cognitive Assessment (MoCA) scores were significantly higher in the triple-agent group ( = 0.002, < 0.001). The dual-agent group had a longer duration of hospitalization but lower average medical costs than the triple-agent group ( = 0.025). No significant difference in 90-day complication incidence was observed between the groups ( > 0.05). At the 90-day follow-up, the triple-agent group demonstrated significantly better upper and lower limb function and higher Barthel scores compared with the dual-agent group ( < 0.001). CONCLUSION: Triple-agent therapy, with alteplase, aspirin, and clopidogrel, may reduce neurological impairment, improve cognitive outcomes, and enhance early functional recovery in patients with stroke, although at the expense of higher medical costs.
Liproxstatin-1 ameliorates cerebral ischemia-reperfusion injury through inhibiting ferroptosis.
Xiong L, Jin Y, Zhang J … +5 more , Shi H, Zhu G, Zhu P, Liu Y, Luo K
Int J Neurosci · 2026 May · PMID 41607012 · Publisher ↗
OBJECTIVE: This study intends to investigate the protective impact of liproxstatin-1 against cerebral ischemia-reperfusion injury (CIRI) in rats and the corresponding underlying mechanism. METHODS: CIRI rat models were c...
OBJECTIVE: This study intends to investigate the protective impact of liproxstatin-1 against cerebral ischemia-reperfusion injury (CIRI) in rats and the corresponding underlying mechanism. METHODS: CIRI rat models were constructed. Pathological changes in tissues were assessed at multiple levels, including infarct area, neuronal activity, and iron content through 2,3,5-triphenyl tetrazolium chloride (TTC) staining, Nissl staining and Prussian blue (PB) staining. The expression of oxidative damage factors and key ferroptosis-related genes was assessed by enzyme-linked immunosorbent assay (ELISA), quantitative real-time PCR (qPCR) or western blot (WB). Rat brain tissues were subjected to bulk RNA sequencing (bulk RNA-seq) analysis. Finally, oxygen-glucose deprivation/reoxygenation (OGD/R) models were established, and the inhibitory effect of liproxstatin-1 on ferroptosis was identified by measuring cell viability, Fe levels and lipid peroxidation. RESULTS: experiments demonstrated that liproxstatin-1 markedly improved neurological function and neuronal pathological damage in CIRI rats, while reducing iron content and oxidative damage. Bulk RNA-seq analysis revealed that differentially expressed genes (DEGs) were mainly enriched in the IL-17 signaling pathway, ether lipid metabolism, TNF signaling pathway and ferroptosis. Consistently, qPCR and WB results showed that liproxstatin-1 treatment increased the expression of FTH1 and GPX4, while decreasing the expression of NOX1, ACSL4, COX2 and TFR1 in rat brain tissues. experiments further demonstrated that liproxstatin-1 significantly enhanced cell viability and reduced Fe and reactive oxygen species (ROS) levels. CONCLUSIONS: Liproxstatin-1 inhibits the process of ferroptosis and alleviates CIRI in rats.
A patent review on traumatic brain injuries (2020-2025).
Sharma K, Agrawal D, Gabrani R
Int J Neurosci · 2026 May · PMID 41572479 · Publisher ↗
INTRODUCTION: Traumatic brain injury (TBI) remains a leading cause of disability and death worldwide, with no FDA-approved therapies capable of halting or reversing secondary injury cascades. AREAS COVERED: Recent years...
INTRODUCTION: Traumatic brain injury (TBI) remains a leading cause of disability and death worldwide, with no FDA-approved therapies capable of halting or reversing secondary injury cascades. AREAS COVERED: Recent years (2020-2025) have witnessed a surge in patent activity targeting diagnostic innovations, biomarker integration, and therapeutic strategies in TBI. Diagnostic advances include multimodal platforms that combine blood-based biomarkers, imaging modalities, and physiological monitoring to enhance early detection and stratification. Biomarker-driven patents, particularly those centered on glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCH-L1), neurofilament light chain (NfL), and p-tau, have demonstrated translational value by enabling point-of-care testing and guiding therapeutic decisions. Therapeutic patents encompass a wide range of innovations, including anti-inflammatory and antioxidant agents, metabolic and vascular stabilizers, regenerative approaches, and advanced drug delivery systems designed to bypass the blood-brain barrier. Importantly, multimodal therapeutic strategies that integrate neuroprotection, neuro-restoration, and functional recovery are gaining momentum. EXPERT OPINION: Innovations in patents, such as breath-based sensors, eye-tracking systems, and non-invasive technologies, are expanding the possibilities for rapid, point-of-care testing. On the therapeutic side, patents focusing on monoclonal antibodies, neuroactive steroids, neuroprotective peptides, and site-specific delivery systems show promise; however, most candidates are still in preclinical or early clinical stages.
Graph-theoretical analysis of resting-state EEG networks differentiates Alzheimer's disease and frontotemporal dementia.
Zhu L, Pan Y, Wang ZL
Int J Neurosci · 2026 May · PMID 41571385 · Publisher ↗
BACKGROUND: Alzheimer's disease (AD) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlapping symptoms, complicating diagnosis. EEG-derived brain connectivity metrics, based on network neuroscien...
BACKGROUND: Alzheimer's disease (AD) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlapping symptoms, complicating diagnosis. EEG-derived brain connectivity metrics, based on network neuroscience, can quantify brain network organization, but comparisons between AD and FTD using standardized EEG datasets are limited. METHODS: We analyzed a publicly available EEG dataset consisting of 36 AD patients, 23 FTD patients, and 29 healthy controls (HCs). Resting-state eyes-closed and eyes-open EEGs were analyzed across delta, theta, alpha, and beta bands. Phase-locking values (PLV) estimated functional connectivity between 19 electrodes, and graph-theory metrics were derived using the Brain Connectivity Toolbox. Group differences were assessed using ANOVAs with FDR correction, followed by Tukey tests. RESULTS: AD patients showed reduced global efficiency and small-worldness, especially in the alpha and beta bands under eyes-closed conditions, indicating decreased integration. FTD patients exhibited localized network disruptions in frontal and central regions, particularly reduced node degree and local efficiency at F3/F4 and Pz electrodes, suggesting region-specific dysfunction. These differences were more prominent in the eyes-closed state. CONCLUSION: EEG graph-theory analysis revealed distinct network alterations in AD and FTD. AD showed impaired global integration and loss of small-world architecture, while FTD demonstrated region-specific disruptions. These findings suggest that EEG graph metrics may serve as cost-effective biomarkers for differentiating dementia subtypes and understanding disease-specific network dysfunction.
FAS rs2234767 polymorphism confers protection against glioma: a case-control study in Chinese population.
Huang X, Ran J, Liang L … +3 more , Li W, Tang J, Ning L
Int J Neurosci · 2026 May · PMID 41569528 · Publisher ↗
BACKGROUND: Genetic polymorphisms in apoptosis-related genes FAS/FASL may influence susceptibility to glioma, but evidence remains limited, particularly in Chinese populations. This study aimed to investigate the potenti...
BACKGROUND: Genetic polymorphisms in apoptosis-related genes FAS/FASL may influence susceptibility to glioma, but evidence remains limited, particularly in Chinese populations. This study aimed to investigate the potential association between gene polymorphisms in FAS (rs2234767 and rs1800682) and FASL (rs763110 and rs6700734) and glioma risk in a Chinese cohort. METHODS: This case-control study included 107 glioma patients and 110 healthy controls. Four polymorphisms were genotyped using TaqMan real-time PCR. The associations between these genetic variants and glioma risk were evaluated logistic regression after adjusting for relevant covariates. Furthermore, subgroup analyses stratified by ethnicity, isocitrate dehydrogenase 1 (IDH1) R132H status and histological grade were performed, along with a haplotype-based analysis. RESULTS: The FAS rs2234767 GA genotype was associated with a significantly reduced glioma risk compared to the GG genotype (adjusted OR = 0.461, 95% CI: 0.232-0.917, = 0.027). This protective effect was particularly evident in the Han subgroup (adjusted OR = 0.275, 95% CI: 0.106-0.716, = 0.008), IDH1 R132H-positive cases (adjusted OR = 0.362, 95% CI: 0.148-0.884, = 0.026) and low-grade gliomas (adjusted OR = 0.350, 95% CI: 0.133-0.922, = 0.034). No notable associations were observed for FASL variants. Haplotype analyses revealed no significant associations. CONCLUSIONS: This study suggests a potential protective role of the FAS rs2234767 GA genotype against glioma in the Chinese population, particularly among Han individuals, IDH1 R132H-positive cases and low-grade gliomas. The findings, while insightful, require validation in larger cohorts. Future research should integrate molecular profiling and functional assays to clarify the underlying mechanisms.
Association between high-density lipoprotein cholesterol to apolipoprotein A-1 ratio and the outcome of ischemic stroke: a retrospective study.
Li L, Deng H, Xu Z … +5 more , Liu Y, Zhang X, Zhou Q, Xiao B, Liu H
Int J Neurosci · 2026 May · PMID 41510695 · Publisher ↗
BACKGROUND: High-density lipoprotein cholesterol (HDL-C)/apolipoprotein A-1 (APOA-1) ratio has been identified as a risk factor for cardiovascular disease, cancer, and all-cause mortality. However, data related to ischem...
BACKGROUND: High-density lipoprotein cholesterol (HDL-C)/apolipoprotein A-1 (APOA-1) ratio has been identified as a risk factor for cardiovascular disease, cancer, and all-cause mortality. However, data related to ischemic stroke (IS) are lacking. We investigated whether the HDL-C/APOA-1 ratio was associated with 3-month functional outcome in patients with IS. METHODS: A retrospective analysis was performed on 674 patients with IS. The 3-month functional outcome was classified as good or poor based on the modified Rankin Scale score (mRS). Logistic regression models (unadjusted and stepwise) were performed to evaluate the correlation between HDL-C/APOA-1 ratio and outcome. Restricted cubic splines evaluated nonlinear relationships, while subgroup analyses explored effect modifications. We assessed the added predictive value of the HDL-C/APOA-1 ratio by comparing nested models using the AUC, NRI, and IDI. RESULTS: The HDL-C/APOA-1 level in the group with poor functional outcomes was higher than that in the group with good functional outcomes (0.99 ± 0.14 vs. 0.94 ± 0.10, < 0.001). In the multivariable analysis, a higher HDL-C/APOA-1 ratio was identified as an independent factor associated with poor outcome at 3 months (OR 1.50, 95% CI:1.17-1.96, = 0.003). The odds of poor outcome in the higher HDL-C/APOA-1 quartile increased by 2.44-fold (95% CI:1.30-4.64, = 0.006) after adjusting for potential confounders compared to lower HDL-C/APOA-1 quartiles. In addition, multivariate-adjusted restricted cubic splines show a positive approach linear pattern of this association. CONCLUSION: Elevated HDL-C/APOA-1 is independently associated with an increased risk of poor functional outcomes at 3-month in patients with IS.
Evolving trends and disparities in malnutrition-linked stroke mortality in the United States: insights from CDC WONDER data.
Sahil FNU, Jairamani S, Cheema MRS … +6 more , Urooba F, Ibrahim M, Abufatima IO, Nawaz A, Sajjad M, Kumar D
Int J Neurosci · 2026 May · PMID 41487015 · Publisher ↗
BACKGROUND: Stroke and malnutrition remain significant contributors to preventable mortality in the United States. Stroke is a leading cause of death and disability, while malnutrition, often underrecognized, exacerbates...
BACKGROUND: Stroke and malnutrition remain significant contributors to preventable mortality in the United States. Stroke is a leading cause of death and disability, while malnutrition, often underrecognized, exacerbates neurological and systemic vulnerability. Characterizing long-term national and subgroup-specific mortality patterns is critical for guiding public health interventions. METHODS: Mortality data for stroke and malnutrition were analyzed from 1999 to 2023 using the CDC WONDER database. Age-adjusted mortality rates (AAMR) per 1,000,000 population were calculated and stratified by sex, race/ethnicity, census region, state and urbanization status. Joinpoint regression estimated average annual percent change (AAPC) with 95% confidence intervals (CIs). RESULTS: From 1999 to 2023, 44,368 deaths were attributed to malnutrition and stroke. The overall AAMR rose from 12.11 in 1999 to 14.75 in 2023, with an overall AAPC of 0.88% (95% CI: -0.14 to 1.91). Males had higher AAMRs than females. By race, Non Hispanic (NH) Black experienced the greatest AAMRs, whereas NH Asian had the lowest rates. Regionally, the South showed the highest rate, whereas Northeast had the lowest. Nonmetropolitan areas exceeded metropolitan areas. At the state level, the highest rates were observed in South Dakota and Arkansas, while Massachusetts recorded the lowest rates. CONCLUSION: From 1999 to 2023, combined mortality from stroke and malnutrition increased modestly nationwide, with enduring disparities across demographics and geography. The highest burdens fell on NH Black individuals, people living in the South and nonmetropolitan areas, and certain central states. These findings highlight the need for region-specific prevention and better access to nutritional and neurological care.
Genetic evidence for the causal relationship between cerebrospinal fluid metabolites and intracranial aneurysms: a bidirectional two-sample Mendelian randomization study.
Xiao R, Zhang W
Int J Neurosci · 2026 May · PMID 41472634 · Publisher ↗
BACKGROUND: Intracranial Aneurysms (IA) are life-threatening cerebrovascular diseases, and their pathogenesis remains not fully understood. This study aims to systematically evaluate the causal relationship between cereb...
BACKGROUND: Intracranial Aneurysms (IA) are life-threatening cerebrovascular diseases, and their pathogenesis remains not fully understood. This study aims to systematically evaluate the causal relationship between cerebrospinal fluid (CSF) metabolites and IA through bidirectional two-sample Mendelian randomization (MR) analysis to identify potential biomarkers and therapeutic targets. METHODS: Using genome-wide association study data from public databases, the primary analysis was conducted with inverse variance weighting, supplemented by MR-Egger regression, weighted median, weighted mode, and simple mode. Sensitivity analyses were performed using heterogeneity tests, horizontal pleiotropy tests, and leave-one-out analyses to ensure the stability of the results. RESULTS: Forward MR analysis revealed that 1-arachidonoyl-gpc (20:4n6), 2'-deoxyuridine, 3-hydroxystachydrine, 5-hydroxyhexanoate, isobutyrylcarnitine (C4), phenylacetylglutamine, and X-10457 were protective factors for IA. In contrast, 2-hydroxybutyrate/2-hydroxyisobutyrate, arabonate/xylonate, argininosuccinate, citrate, cysteinylglycine disulfide, and isovalerate were identified as risk factors for IA. Reverse MR analysis showed a significant causal relationship between IA and changes in the concentrations of 14 CSF metabolites. Sensitivity analyses indicated the robustness of these findings. CONCLUSIONS: This study, through bidirectional MR analysis, uncovered the causal relationship between CSF metabolites and IA, highlighting the significant roles of various amino acids and lipid metabolites in the pathophysiology of IA. These metabolites not only provide new insights into the mechanisms underlying IA but also present potential biomarkers and therapeutic targets, offering theoretical support for early intervention and prevention strategies for the disease.
Beyond the impact: emerging therapies shaping the future of post-concussion recovery.
Raza ML, Hassan ST, Fatima W … +2 more , Hyder N, Turabee Z
Int J Neurosci · 2026 May · PMID 41457287 · Publisher ↗
Persistent post-concussion symptoms can greatly affect a person's life, thinking abilities, and their capacity to go back to normal daily tasks. This narrative review gives a detailed look at new treatments for ongoing s...
Persistent post-concussion symptoms can greatly affect a person's life, thinking abilities, and their capacity to go back to normal daily tasks. This narrative review gives a detailed look at new treatments for ongoing symptoms after a concussion. It includes methods like brain stimulation, medications, and holistic approaches. We searched for information using PubMed, Embase, and Google Scholar, looking for keywords like 'post-concussion syndrome', 'neuromodulation', 'rehabilitation', 'cognitive behavioral therapy', 'vestibular therapy', and 'medications. 'This review talks about how each therapy works, the proof from clinical trials, and practical tips for using them. Methods like transcranial magnetic stimulation and transcranial direct current stimulation could help improve thinking skills and mood problems. Medicines like amantadine and zolpidem may help treat certain symptoms. Methods like aerobic exercise, balance training, and talk therapy provide overall benefits. The review also points out future areas to explore, like stem cell treatment, using virtual reality for rehab, timing treatments better, and using light therapy. This review looks at new information and trends to help doctors and researchers understand the latest ways to treat ongoing symptoms after a concussion. It also aims to guide future studies in this important field.
Lactate dehydrogenase-to-albumin ratio predicts ischemic stroke recurrence in patients with symptomatic carotid artery stenosis: a pilot retrospective cohort study.
Ye F, Ren N, Fang H … +1 more , Shen K
Int J Neurosci · 2026 May · PMID 41403241 · Publisher ↗
AIM: Symptomatic carotid artery stenosis (SCAS) patients face a high risk of ischemic stroke (IS) recurrence. This study evaluates the prognostic value of the serum lactate dehydrogenase (LDH)-to-albumin ratio (L/A) for...
AIM: Symptomatic carotid artery stenosis (SCAS) patients face a high risk of ischemic stroke (IS) recurrence. This study evaluates the prognostic value of the serum lactate dehydrogenase (LDH)-to-albumin ratio (L/A) for predicting IS recurrence among SCAS patients. METHODS: In this retrospective study (January 2020-January 2023), 307 conservatively managed SCAS patients were stratified into non-recurrence ( = 238) and recurrence ( = 69) groups based on 24-month follow-up. Serum LDH and albumin were measured, and L/A was calculated. Relationships between L/A and plaque neovascularization-related parameters (peak intensity, AUCTC, CAS rate) were assessed using Pearson correlation. Independent risk factors were determined with multivariate Cox regression, while the predictive performance and risk stratification of L/A were evaluated with ROC and Kaplan-Meier curves. RESULTS: Significant differences existed in age, hypertension, hyperlipidemia, systolic blood pressure, low-density lipoprotein cholesterol, albumin, peak intensity, AUCTC, CAS rate, vulnerable plaques, and medication adherence between the two groups. Recurrent patients exhibited higher L/A ( < 0.005). L/A correlated positively to peak intensity ( = 0.323), AUCTC ( = 0.450), and CAS rate ( = 0.529; all < 0.001). Hyperlipidemia, vulnerable plaques, peak intensity, CAS rate, and elevated L/A were independent risk factors for IS recurrence in SCAS patients. L/A could assist in predicting IS recurrence in SCAS patients (AUC: 0.801; sensitivity: 63.77%; specificity: 85.71%). High L/A significantly increased 2-year recurrence risk in SCAS patients. CONCLUSION: Elevated L/A potentially aids in predicting IS recurrence in SCAS patients and correlates to plaque neovascularization.
Bioinformatic identification and clinical validation of VIM and OSM as prognostic biomarkers in cerebral infarction: implications for risk stratification.
Fan C, Li C, Sui C … +2 more , Han L, Liu Y
Int J Neurosci · 2026 May · PMID 41368838 · Publisher ↗
BACKGROUND: Reliable molecular biomarkers for predicting cerebral infarction outcomes remain limited, highlighting the need for integrative approaches that bridge bioinformatic discovery with clinical validation. OBJECTI...
BACKGROUND: Reliable molecular biomarkers for predicting cerebral infarction outcomes remain limited, highlighting the need for integrative approaches that bridge bioinformatic discovery with clinical validation. OBJECTIVE: To identify key differentially expressed genes (DEGs) prognostic for cerebral infarction and evaluate their clinical utility for risk stratification through integrated bioinformatic analysis and prospective cohort validation. METHODS: Functional annotation employed GO enrichment and protein-protein interaction network analysis. A prospective cohort enrolled 151 cerebral infarction patients, with peripheral blood samples subjected to qPCR analysis of candidate genes. Prognostic predictive capacity was assessed multivariable Cox regression, Kaplan-Meier survival analysis, and ROC curve analysis with clinical follow-up data. RESULTS: Five candidate DEGs (VIM, OSM, PTGS2, SOD2, SAMSN1) were identified, enriched in inflammatory response, nitric oxide metabolism, and lipopolysaccharide response pathways. qPCR confirmed significantly elevated VIM, OSM, and PTGS2 expression in poor prognosis group ( < 0.01). Multivariable Cox regression identified VIM (HR = 4.475), OSM (HR = 2.800), and homocysteine (Hcy; HR = 1.120) as independent prognostic risk factors. Kaplan-Meier analysis demonstrated significantly reduced survival in high-expression groups (all < 0.01). The combined model integrating VIM, OSM, and Hcy achieved superior predictive performance (AUC = 0.811; sensitivity 72.55%, specificity 78.00%, Youden's index 0.506) compared to VIM alone (AUC = 0.760). CONCLUSION: VIM and OSM exhibit robust bioinformatic associations and stable expression with independent prognostic value in clinical cohorts.
Association of intracranial atherosclerotic plaque features with total cerebral small vessel disease burden: a retrospective study in branch atheromatous disease.
Zhang G, Luo W, Dong Y … +5 more , Wang J, Bu W, Meng D, Meng L, Ren H
Int J Neurosci · 2026 May · PMID 41345539 · Publisher ↗
OBJECTIVE: We investigated the association between middle cerebral artery atherosclerotic plaque features and cerebral small vessel disease (CSVD) imaging markers as well as the total CSVD burden, in patients with branch...
OBJECTIVE: We investigated the association between middle cerebral artery atherosclerotic plaque features and cerebral small vessel disease (CSVD) imaging markers as well as the total CSVD burden, in patients with branch atheromatous disease (BAD). METHODS: Plaque parameters were quantified using high-resolution magnetic resonance imaging (HR-MRI) with ImageJ software, to characterize distribution, lumen stenosis, remodeling patterns, and other relevant features. Conventional MRI assessed CSVD imaging markers and total CSVD burden. Multivariate logistic regression analysis was performed following adjustment for potential confounders. Receiver operating characteristic (ROC) curve analysis with the DeLong test assessed the predictive value of plaque features for total CSVD burden. RESULTS: Compared with the non-plaque group, the plaque group showed significantly higher proportions of severe white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and moderate-to-severe CSVD burden ( < 0.05). In multivariate analysis, the presence of plaque was an independent risk factor for WMHs (OR = 2.920), CMBs (OR = 1.995), and moderate-to-severe CSVD burden (OR = 2.853); plaque distribution was an independent risk factor for WMHs (OR = 3.367); eccentric plaques were independent risk factors for lacunar infarction (OR = 8.670) and CMBs (OR = 7.891); positive remodeling (OR = 9.285) and eccentric plaques (OR = 10.355) were independent risk factors for moderate-to-severe CSVD burden. ROC analysis demonstrated plaque vulnerability effectively predicted moderate-to-severe CSVD burden (AUC = 0.8808, < 0.05). CONCLUSION: In ischemic stroke patients, distinct intracranial atherosclerotic stenosis (ICAS) plaque features correlate with specific CSVD phenotypes. Vulnerable plaques not only significantly increase total CSVD burden but also effectively predict CSVD severity. These findings elucidate how ICAS influences CSVD burden progression from an HR-MRI perspective and facilitate clinical risk stratification.
Unraveling the molecular landscape of ischemic stroke: a bioinformatics approach to identify key genes and therapeutic targets.
Mirtooni SS, Sasannejad P, Rezaeitalab F … +4 more , Gholamian MR, Saeedi M, Tolou V, Amerizadeh F
Int J Neurosci · 2026 Apr · PMID 41275377 · Publisher ↗
BACKGROUND: Ischemic stroke, a major cause of disability and death, results from blocked cerebral blood flow, causing neuronal damage. Limited treatments necessitate research into molecular mechanisms for targeted therap...
BACKGROUND: Ischemic stroke, a major cause of disability and death, results from blocked cerebral blood flow, causing neuronal damage. Limited treatments necessitate research into molecular mechanisms for targeted therapies. METHODS: In this study, we analyzed transcriptomic data from the Gene Expression Omnibus (GEO) database (GSE36010), focusing on gene expression changes in the core region of the brain 24 h post-stroke induction. Enrichment analysis of differentially expressed genes (DEGs) was conducted using Enrichr, exploring Gene Ontology (GO) terms and Reactome pathways. A protein-protein interaction network (PPIN) was constructed using STRING, and hub genes were identified through the CytoHubba plugin in Cytoscape. Network clustering analysis was performed using the iterative partition-based clustering algorithm (IPCA) in CytoCluster. Promoter motif analysis of hub genes was conducted using TomTom and GO for motifs (GOMO), while DrugBank analysis was used to identify potential therapeutic compounds targeting the identified hub proteins.A total of 150 DEGs were identified in the core region of ischemic stroke, with significant enrichment in pathways related to inflammation, oxidative stress, apoptosis and vascular remodeling. Key hub genes like cluster of differentiation 68 (Cd68), chemokine (C-C motif) ligand 3 (Ccl3), transforming growth factor beta 1 (Tgfb1), cluster of differentiation 44 (Cd44), Lgals3, topoisomerase II alpha (Top2a), lipocalin 2 (Lcn2), chemokine (C-C motif) ligand 4 (Ccl4), Ckap2 and cell division cycle associated 2 (Cdca2) were found to play critical roles in neuronal survival, inflammation and vascular integrity. Additionally, drug analysis highlighted several FDA-approved drugs that could be repurposed for stroke therapy, emphasizing the potential therapeutic candidates targeting these hub proteins. CONCLUSION: This study analyzes ischemic stroke, identifying key pathways and drug targets, potentially aiding in developing targeted therapies to reduce damage and improve outcomes for stroke patients.
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