International Journal of Neuroscience最新文献

{"title":"Chronic 40-hz light-emitting diode (LED) therapy attenuates cognitive and behavioral deficits and modulates BDNF and caspase-3 expression in a D-galactose/aluminum chloride-induced sporadic Alzheimer's-like rat model.","authors":"Elham Ghorbani, Saeed Hajihashemi, Javad Fahanik-Babaei, Maryam Nazari","doi":"10.1080/00207454.2026.2706611","DOIUrl":"10.1080/00207454.2026.2706611","url":null,"abstract":"<p><strong>Introduction: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by gradual deterioration of cognition, synaptic integrity, and neuronal viability. Experimental exposure to D-galactose (D-gal) combined with aluminum chloride (AlCl₃) produces oxidative and inflammatory damage within the brain, closely resembling AD-related neuropathology. Photobio-modulation therapy (PBMT) has recently gained attention as a safe, non-pharmacological approach with neuroprotective potential; however, the impact of sustained 40-Hz light-emitting diode (LED) stimulation in this context remains insufficiently explored.</p><p><strong>Methods: </strong>In the present study, rats received D-gal (60 mg/kg, i.p.) and AlCl₃ (200 mg/kg, oral) for six weeks to induce AD-like changes. The treatment group was exposed to 40-Hz pulsed LED light (425-550 nm, 15 min/session, three times weekly). Behavioral analyses were performed using the elevated plus maze (EPM), novel object recognition (NOR), and passive avoidance (PA) paradigms. Western blotting quantified brain-derived neurotrophic factor (BDNF) and cleaved-caspase-3 expression in whole brain tissue.</p><p><strong>Results: </strong>D-gal/AlCl₃ administration produced anxiety-like behavior, recognition deficits, and impaired memory retention, accompanied by decreased BDNF and elevated caspase-3. Remarkably, 40-Hz LED exposure reversed these alterations, up-regulating BDNF and suppressing caspase-3, in parallel with improvements in cognitive and emotional outcomes.</p><p><strong>Conclusion: </strong>These data suggest that 40-Hz LED stimulation confers neuroprotection in the D-gal/AlCl₃-induced AD model, potentially through enhancement of neurotropic signaling and inhibition of apoptosis, supporting its promise as a non-invasive strategy against neurodegenerative decline.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1400-1412"},"PeriodicalIF":1.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A predictive model for early neurological deterioration in medullary infarction based on explainable machine learning.","authors":"Binger Fan, Yanjiao Guan, Linhu Zhao, Hongli Liu, Gang Tang, Chunyan Lei, Ansong Jin, Xiaoyan Zhu, Ruohong Xue, Xinglong Yang","doi":"10.1080/00207454.2026.2697821","DOIUrl":"10.1080/00207454.2026.2697821","url":null,"abstract":"<p><strong>Background: </strong>Medullary infarction is a severe subtype of ischemic stroke. Early neurological deterioration (END) is a common adverse event that can significantly affect clinical outcomes.</p><p><strong>Objective: </strong>This study aimed to develop a machine learning model to effectively predict the risk of END in patients with medullary infarction, thereby providing a reference for clinical intervention.</p><p><strong>Methods: </strong>In this multicenter retrospective study, we enrolled patients with acute medullary infarction who received treatment at three hospitals located in different regions between 2019 and October 2024. We collected comprehensive, multi-dimensional clinical data and employed five distinct algorithms to construct predictive models. The performance of these models was thoroughly evaluated using accuracy, area under the receiver operating characteristic curve (AUC), precision-recall curves, and calibration curves.</p><p><strong>Results: </strong>A total of 352 patients were enrolled in this study. The incidence of END was 10% (35), while the incidence of non-END was 90% (317). Seven features were used to build prediction models with the five algorithms. The single-layer neural network demonstrated superior performance in predicting END, achieving an AUC of the receiver operating characteristic (ROC) curve of 0.873 on the validation set, while also exhibiting favorable calibration and a balanced overall performance profile. In comparison, the Naïve Bayes model showed excellent classification consistency and may serve as a complementary tool in clinical practice.</p><p><strong>Conclusion: </strong>This study developed a highly accurate single-layer neural network and a robust Naïve Bayes classifier, which together provide an interpretable tool for assessing the risk of END in stroke patients across various clinical settings.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1362-1368"},"PeriodicalIF":1.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recurrence associated IGFBP2 promotes malignant progression and epithelial mesenchymal transition in glioma cells via the AKT mTOR pathway.","authors":"Yuxuan Que, Wenxuan Zhao, Bao He","doi":"10.1080/00207454.2026.2693881","DOIUrl":"10.1080/00207454.2026.2693881","url":null,"abstract":"<p><strong>Background: </strong>Glioma recurrence and progression are major causes of poor prognosis and death. Although surgery can provide short-term benefit, long-term outcomes remain limited because effective targets for preventing recurrence and progression are lacking.</p><p><strong>Methods: </strong>Differentially expressed genes between primary and recurrent gliomas were identified using the CGGA and TCGA databases. The effects of IGFBP2 knockdown on glioma cell proliferation, colony formation, migration, and invasion were assessed by CCK-8, colony formation, migration, and invasion assays. Western blotting was used to investigate the underlying molecular mechanisms.</p><p><strong>Results: </strong>Bioinformatics analysis identified IGFBP2 as a recurrence-associated candidate gene in glioma. High IGFBP2 expression was associated with recurrence status and shorter overall survival. <i>In vitro</i> experiments showed that IGFBP2 knockdown suppressed glioma cell proliferation, colony formation, migration, and invasion. Mechanistically, IGFBP2 knockdown was accompanied by changes in EMT-related markers and reduced AKT/mTOR signaling activity.</p><p><strong>Conclusion: </strong>IGFBP2 may serve as a recurrence-associated candidate biomarker and potential therapeutic target in glioma. Further validation using clinical specimens, patient-derived models, orthotopic animal models, and mechanistic rescue experiments is required to confirm its biological and translational significance.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1330-1343"},"PeriodicalIF":1.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic value of miR-34c-5p in acute cerebral infarction and its correlation with prognostic outcomes of rehabilitation.","authors":"Hongjie Jiang, Xin Zhang, Wei Wang, Shasha Wang, Yingming Xie, Yingbin Xue, Junyao Song, Xiumei Hu","doi":"10.1080/00207454.2026.2697818","DOIUrl":"10.1080/00207454.2026.2697818","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore the role of miR-34c-5p in ACI to provide novel insights for ACI clinical management.</p><p><strong>Methods: </strong>This study enrolled 376 subjects (176 healthy individuals, 200 ACI patients). Serum miR-34c-5p expression was quantified by qRT-PCR, with its diagnostic potential evaluated by receiver operator characteristic (ROC) curve. The association between miR-34c-5p and ACI severity was evaluated by correlation analysis. Dual-luciferase assay validated miR-34c-5p/FOSL1 interaction. An oxygen-glucose deprivation and reperfusion (OGD/R)-induced SH-SY5Y model was employed for evaluating the effect of miR-34c-5p/FOSL1 axis on cerebral ischemia-reperfusion injury (CIRI).</p><p><strong>Results: </strong>MiR-34c-5p downregulation possessed a diagnostic potential in ACI. The miR-34c-5p expression, negatively correlating with the NIHSS scores of ACI subjects, was lower in ACI subjects with moderate/severe severity and unfavorable prognosis. MiR-34c-5p downregulation and higher NIHSS scores were risk factors for ACI poor prognosis. OGD/R reduced cell viability, facilitated inflammation (IL-6, TNF-α), and oxidative stress (decreased SOD activity, increased MDA level) in SH-SY5Y cells. MiR-34c-5p overexpression protected against OGD/R-induced SH-SY5Y injury by improving viability, suppressing inflammation, and oxidative stress <i>via</i> targeting FOSL1.</p><p><strong>Conclusions: </strong>Downregulation of miR-34c-5p showed a diagnostic potential on ACI and was correlated with ACI severity and prognosis.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1352-1361"},"PeriodicalIF":1.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astaxanthin alleviates ischemia-reperfusion injury by regulating the JAK2/STAT3 signaling pathway.","authors":"Yuhong Zhang, Jingxi Jiang, Zhenhuan Ma, Hong Gong","doi":"10.1080/00207454.2026.2690251","DOIUrl":"10.1080/00207454.2026.2690251","url":null,"abstract":"<p><strong>Background: </strong>Cerebral ischemia-reperfusion injury (CIRI) lacks effective treatments. Astaxanthin (AST) ameliorates CIRI, but the underlying mechanisms remain unclear.</p><p><strong>Methods: </strong>An oxygen-glucose deprivation/reoxygenation (OGD/R) model in PC12 cells and a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model were used. Cell viability (MTT), apoptosis (flow cytometry), oxidative damage (8-OHdG, 4-HNE, MDA, ROS), inflammatory factors (TNF-α, IL-1β, IL-6, MCP-1), and JAK2/STAT3 pathway proteins (p-JAK2, p-STAT3) were assessed, with or without AST treatment and JAK2 agonist intervention.</p><p><strong>Results: </strong>OGD/R significantly reduced PC12 cell viability, increased apoptosis, and elevated oxidative and inflammatory markers, while activating JAK2/STAT3. AST treatment reversed these effects-promoting proliferation, inhibiting apoptosis, and reducing damage markers. AST also suppressed p-JAK2 and p-STAT3 expression. Activation of the JAK2/STAT3 pathway abolished AST's protective effects against OGD/R-induced damage. In vivo, AST effectively alleviated ischemia-reperfusion injury in rats.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1295-1307"},"PeriodicalIF":1.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148271404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined assessment of established biomarkers: monocyte-to-HDL ratio and carotid IMT in association with acute ischemic stroke.","authors":"Yin Tongtong, Wang Qian, Liu Ziyi, Wang Chengxue, Li Xiumei, Dong Zuoliang, Luo Wei","doi":"10.1080/00207454.2026.2719584","DOIUrl":"10.1080/00207454.2026.2719584","url":null,"abstract":"<p><strong>Aim: </strong>Inflammation is strongly linked to atherosclerosis and acute ischemic stroke (AIS). This study investigated the association of the monocyte-to-HDL ratio (MHR), an inflammatory marker, and common carotid artery intima-media thickness (CCA-IMT), a measure of atherosclerosis, both individually and in combination, with AIS.</p><p><strong>Methods: </strong>This case-control study included 533 AIS patients and 218 healthy controls. MHR and CCA-IMT levels were compared between groups. Associations with AIS were analyzed using multivariate logistic regression, and discriminative performance was evaluated by receiver operating characteristic (ROC) curve analysis. The correlation between MHR and CCA-IMT was assessed using Pearson's correlation coefficient.</p><p><strong>Results: </strong>MHR and CCA-IMT were significantly higher in AIS patients than controls (both <i>p</i> < 0.05). Both remained independently associated with AIS after adjusting for confounders. The area under the curve (AUC) was 0.719 for MHR, 0.928 for CCA-IMT, and 0.940 for their combination. MHR was positively correlated with CCA-IMT in AIS patients (<i>r</i> = 0.386, <i>p</i> < 0.001).</p><p><strong>Conclusions: </strong>MHR and CCA-IMT were independently associated with AIS, and their combination demonstrated high discriminatory ability in distinguishing AIS patients from healthy controls, with CCA-IMT as the dominant discriminator and MHR providing complementary inflammatory information. These findings are consistent with the proposed \"inflammation-atherosclerosis axis\" in AIS pathogenesis.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1-13"},"PeriodicalIF":1.7,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction.","authors":"","doi":"10.1080/00207454.2026.2683282","DOIUrl":"10.1080/00207454.2026.2683282","url":null,"abstract":"","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1"},"PeriodicalIF":1.7,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148721528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Purinergic signaling: a novel therapeutic target in depression.","authors":"Qianqian Cui, Yunxiao Li, Shuangqi Gao, Haiyun Zhou, Yan Peng","doi":"10.1080/00207454.2026.2666245","DOIUrl":"10.1080/00207454.2026.2666245","url":null,"abstract":"<p><p>Major depressive disorder, as a common neuropsychiatric disorder, has a complex pathogenesis that has not yet been fully elucidated, posing significant challenges to clinical treatment. In recent years, the role of the purinergic signaling system in the pathophysiological processes of depression has garnered increasing attention. The purinergic signaling primarily involves extracellular purine compounds such as ATP and adenosine, which act as transmitters by binding to their corresponding purine receptors (P1 and P2). Purinergic signaling can participate in depression by affecting the function of astrocytes, neuronal plasticity, and the activity of microglia. This paper systematically reviews the latest research advancements in purinergic signaling related to depression by searching for articles on the PubMed using the keywords 'purinergic' OR 'ATP' OR 'adenosine' and 'depression'. It focuses on the molecular mechanisms of action and discusses the limitations and controversial issues present in current research, aiming to provide new theoretical foundations and treatment strategies for the precise treatment of depression.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1258-1270"},"PeriodicalIF":1.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bobcat-optimized hybrid quantum-classical spike-driven network for MRI-based Alzheimer's stage prediction.","authors":"Dinesh G, Padmanaban K, Rajeshkannan S, T R Vijaya Lakshmi","doi":"10.1080/00207454.2026.2683880","DOIUrl":"10.1080/00207454.2026.2683880","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that severely affects memory, cognition, and behavioral functions, making early and accurate stage classification essential for timely clinical intervention and treatment planning. Conventional MRI-based diagnostic approaches are often limited by noise sensitivity, manual interpretation, and insufficient capability to model complex non-linear neuroimaging relationships across multiple disease stages. To address these limitations, this paper proposes a novel Hybrid Quantum-Classical Spike-Driven Network optimized with the Bobcat Optimization Algorithm(HQSDNet-BOA)for automated multistage AD classification using MRI data. The suggested framework introduces an integrated architecture that combines Square Root Sage-Husa Adaptive Robust Kalman Filtering(SRS-HARKF)for adaptive noise suppression and covariance stabilization, Graph-Enhanced Fuzzy Clustering (GEFC)for structurally consistent brain tissue segmentation, and a Hybrid Structural Graph Attention Network(HSGAN)for learning discriminative local-global anatomical representations. Moreover, Hybrid Quantum-Classical Spike-Driven Network (HQSDNet), which incorporates quantum convolutional learning, spike-driven transformers, and structural attention schemes, is designed to precisely identify nonlinear and spatial-temporal disease patterns. Bobcat Optimization Algorithm (BOA) is used for optimizing network parameters in real-time to ensure convergence efficiency and computational optimization. This study was performed using two datasets: ADNI (5,300 images representing five disease stages) and OASIS-3 (3,712 images representing three cognitive classes). The suggested HQSDNet-BOA yielded improved classification results with 98.8% accuracy, 98.0% precision, 98.5% recall, and 98.25% F1-score when applied to the ADNI dataset and outperformed the existing techniques in terms of computational speed. The obtained results confirm that the suggested framework provides a robust, efficient, and clinically relevant solution for accurate AD stage prediction and neuroimaging-based diagnostic support.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1134-1158"},"PeriodicalIF":1.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased miR-1305 expression is associated with tumour invasiveness and poor prognosis in glioma patients.","authors":"Yong Wang, Mengnan Guo","doi":"10.1080/00207454.2026.2686992","DOIUrl":"10.1080/00207454.2026.2686992","url":null,"abstract":"<p><strong>Introduction: </strong>Gliomas are highly prevalent and lethal primary malignant tumours of the central nervous system. MicroRNA plays a tumour-suppressive role in various tumours, including glioma. This study aims to elucidate the expression profile, clinical relevance, biological roles, and underlying mechanisms of miR-1305 in glioma.</p><p><strong>Methods: </strong>Tumour tissues alongside their matched normal counterparts were acquired from 105 individuals with glioma. The expression of miR-1305 was quantified using RT‑qPCR. The relationship between miR-1305 expression, clinicopathological characteristics, and prognosis was assessed through Kaplan‑Meier analysis and Cox regression. The proliferative, migratory, and invasive capacities of glioma cells following miR-1305 modulation were assessed using CCK‑8 and Transwell assays. Potential target genes of miR-1305 were predicted <i>via</i> bioinformatics analysis, and the direct targeting interactions were subsequently confirmed by dual-luciferase reporter assays.</p><p><strong>Results: </strong>A significant downregulation of miR-1305 was observed in glioma tissues. Low expression of miR-1305 was associated with increased tumour size, poorer KPS score, and higher WHO tumour grade (<i>p</i> < 0.05). Patients exhibiting low miR-1305 levels experienced decreased overall survival; multivariate analysis identified this marker as an independent prognostic factor. Functional assays showed miR-1305 overexpression inhibited glioma cell proliferation, migration, and invasion. Mechanistically, WNK3 was a direct target of miR-1305, exhibited inverse correlation in glioma, and its overexpression rescued miR-1305-mediated suppression of malignant phenotypes.</p><p><strong>Conclusion: </strong>Low miR-1305 expression is associated with an adverse prognosis in glioma; it exerts tumour-suppressive effects by targeting WNK3 and inhibiting disease progression.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1184-1193"},"PeriodicalIF":1.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}