AIM:To translate the National Institute of Neurological Disorders and Stroke (NINDS) neural exposome framework into a clinically measurable model for 6-month cognitive trajectory after mild traumatic brain injury (mTBI) using principal component analysis (PCA). METHODS:Forty-four adults with mTBI (GCS 13-15; 50% female) were prospectively enrolled at an academic TBI clinic. Fifteen a priori variables spanning Exogenous, Endogenous, and Behavioral exposure categories were assessed. First, an outcome-informed forward-selection procedure identified a coherent 13-variable exposome set, summarized using PCA to derive a cumulative exposome burden score. Cognitive outcome was defined by residualized 6-month Montreal Cognitive Assessment (MoCA) performance dichotomized into worse-than-expected (WTE; ≤ -1 point) and not-worse-than-expected (nWTE) recovery groups. Second, separate PCA analyses were performed within each exposure category, without reference to cognitive outcome, to evaluate internal coherence and directional associations with cognitive recovery. RESULTS:Cross-category PCA identified a latent exposome axis explaining 16.0% of overall variance, driven primarily by education, area deprivation, insurance coverage, PM2.5 exposure, and adverse childhood events. Cumulative exposome burden scores were significantly higher in the WTE group (n = 15) versus nWTE (n = 29) (median PC1: 1.34 vs -0.76; p = 0.010), with similar findings on permutation testing (p = 0.037). Category-level PCA demonstrated coherent internal structure, with first principal components explaining 30.1% (Exogenous), 34.7% (Endogenous), and 39.7% (Behavioral) of within-category variance. Associations with residualized 6-month MoCA were directionally negative across all three categories. CONCLUSIONS:Neural exposome burden composites stratified 6-month cognitive trajectories after mTBI. Coherent PCA structure across NINDS-informed exposure categories supports the feasibility of exposome-informed approaches for post-mTBI cognitive risk stratification.
AIM: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. METHODS: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. RESULTS:MHR and CCA-IMT were significantly higher in AIS patients than controls (both p < 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 (r = 0.386, p < 0.001). CONCLUSIONS: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.
Aquaporin channels are the predominant fluid regulating channel found in the central nervous system (CNS) and plays a pivotal role in maintaining fluid and ion homeostasis, as well as regulating neuroinflammation, neurodegeneration, and blood-brain barrier (BBB) disruption. This protein is primarily located at astrocytes endfeet within the blood cerebral barrier and other central nervous system (CNS) junctions, facilitating the movement of water in both directions, buffering potassium levels, and aiding in the clearance of interstitial solutes, along with toxic metabolites such as amyloid-β, via the glymphatic system. Changes in the expression or polarization of AQPs are implicated in neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, epilepsy, and ischemic stroke. Impaired functionality of AQPs is involved in a number of pathological processes including heightened oxidative stress, disruption of the blood-brain barrier, and neuroinflammation. Such pathways are targeted by transcription factors, including nuclear factor κB (NFκB), and signaling pathways, including p38 MAPK, that increase AQPs expression following the action of stressors. Furthermore, impairment of AQPs polarity suppresses glymphatic clearance and promotes toxic protein accumulation, one of the key features of Alzheimer 's disease. AQPs structural features, including its six transmembrane helices and conserved NPA motifs, are critical for function, positioning it as a putative therapeutic target. Preclinical data support the notion that modulation of AQPs activity may offer neuroprotection through restoration of homeostasis and reduction of inflammation in neurodegenerative disease. This review describes the mechanistic links between AQPs dysfunction and neurodegenerative disease, highlighting its potential and limitations as a therapeutic target for the prevention of CNS disorders.
OBJECTIVE:Propofol is a widely administered anesthetic agent given intravenously. This study investigated the function of miR-4508 within propofol-elicited neurotoxicity in SH-SY5Y cells, identified its downstream target genes, and elucidated the underlying molecular regulatory pathway. METHODS:Propofol neurotoxicity was modeled in SH-SY5Y cells with varying concentrations and durations. Cell viability, miR-4508, oxidative stress, and inflammatory cytokines were measured. Target prediction and dual-luciferase validation, along with miRNA inhibitor and rescue experiments, were used to elucidate the regulatory mechanism. Cognitive function and hippocampal miR-4508 expression were also preliminarily assessed in propofol-exposed mice using the Morris water maze and RT-qPCR, respectively. RESULTS:Propofol reduced SH-SY5Y cell viability and upregulated miR-4508 in a manner dependent on both concentration and time, peaking at 50 μM for 24 h. Five candidate targets were identified bioinformatically. PLCB2 was most downregulated by miR-4508 overexpression. A dual-luciferase assay verified that miR-4508 directly binds to the PLCB2 3'-UTR. A miR-4508 inhibitor attenuated propofol-induced oxidative stress and inflammation, effects reversed by PLCB2 knockdown. Preliminary in vivo observations suggested impaired learning/memory and increased hippocampal miR-4508 in propofol-treated mice, with miR-4508 inhibition showing a tendency toward reversal of these deficits, though further validation is required. CONCLUSIONS:This study demonstrates that propofol upregulates miR-4508 to suppress PLCB2, driving oxidative stress and neuroinflammation. Forward and reverse rescue experiments confirm the miR-4508/PLCB2 axis as a potential therapeutic target for propofol-induced neurotoxicity.
OBJECTIVE:This study aimed to explore the role of miR-34c-5p in ACI to provide novel insights for ACI clinical management. METHODS: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). RESULTS: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 via targeting FOSL1. CONCLUSIONS:Downregulation of miR-34c-5p showed a diagnostic potential on ACI and was correlated with ACI severity and prognosis.
INTRODUCTION: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. METHODS: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. RESULTS: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. CONCLUSION: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.
BACKGROUND:Glioblastoma (GBM) has an extremely poor prognosis, and its malignant progression is closely associated with glutamine metabolic reprogramming and immune evasion; however, the key regulatory networks remain unclear. METHODS:This study integrated bioinformatics data and identified key proteins through weighted gene co-expression network analysis (WGCNA), screening for differentially expressed proteins (DEPs), and machine learning algorithms. The functions and molecular mechanisms were validated using in vitro cell experiments and in vivo mouse models. RESULTS:Oxoglutarate dehydrogenase L (OGDHL) was identified as the key protein in GBM. It was down-regulated in both GBM and low-grade glioma (LGG) tissues and was correlated with immune cell infiltration. OGDHL overexpression inhibited GBM cell proliferation and reduced glutamate, α-ketoglutarate (α-KG), lactate production, and programmed death-ligand 1 (PD-L1) expression, while promoting apoptosis. OGDHL overexpression enhanced CD8+ T cell-mediated cytotoxicity and interferon-γ (IFN-γ) secretion. Mechanistically, OGDHL overexpression suppressed histone H3 lysine 18 lactylation (H3K18la) enrichment, reduced luciferase activity, and inhibited PD-L1 expression in GBM cells, effects that were rescued by exogenous lactate supplementation. In vivo, OGDHL up-regulation inhibited tumor growth, reduced glutamate and lactate production, and decreased Ki-67- and PD-L1-positive cells, while increasing OGDHL-positive cells. CONCLUSION:OGDHL exerts a tumor-suppressive function in GBM by regulating glutamine metabolism and histone lactylation-mediated PD-L1 expression, representing a potential new target for immunometabolic therapy.
OBJECTIVE:This work was conducted to evaluate the effects of thoracic paravertebral nerve block (TPVB) combined with general anesthesia (GA) on pain and lumbar function in patients undergoing minimally invasive vertebroplasty. METHODS:One hundred patients scheduled for minimally invasive vertebroplasty were randomly allocated to a GA group (GA alone, n = 50) or a TPVB + GA group (TPVB combined with GA, n = 50). Mean arterial pressure (MAP) and heart rate (HR) were recorded preoperatively (T0), at puncture (T1), at bone cement injection (T2), and at the end of surgery (T3). Operative time, intraoperative blood loss, and anesthetic consumption were compared. Pain was assessed using the visual analogue scale (VAS) on postoperative days 1, 3, and 7. Lumbar function was evaluated using the Oswestry Disability Index (ODI) preoperatively, 1 week postoperatively, and 1 month postoperatively. Adverse events were also recorded. RESULTS:Significant group, time, and interaction effects were observed for MAP, HR, VAS, and ODI (all p < 0.05). Compared with the GA group, the TPVB + GA group showed lower MAP and HR at T1-T3, reduced blood loss and anesthetic use, lower VAS scores, improved ODI scores, and fewer adverse events (all p < 0.05). CONCLUSION:TPVB combined with GA stabilizes perioperative hemodynamics, alleviates pain, and promotes recovery of lumbar function.
Background 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.Methods 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.Results Bioinformatics analysis identified IGFBP2 as a recurrence-associated candidate gene in glioma. High IGFBP2 expression was associated with recurrence status and shorter overall survival. In vitro 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.Conclusion 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.
INTRODUCTION: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. METHODS: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 via bioinformatics analysis, and the direct targeting interactions were subsequently confirmed by dual-luciferase reporter assays. RESULTS: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 (p < 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. CONCLUSION:Low miR-1305 expression is associated with an adverse prognosis in glioma; it exerts tumour-suppressive effects by targeting WNK3 and inhibiting disease progression.
BACKGROUND:Cerebral ischemia-reperfusion injury (CIRI) lacks effective treatments. Astaxanthin (AST) ameliorates CIRI, but the underlying mechanisms remain unclear. METHODS: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. RESULTS: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.
AIM:To compare the clinical efficacy and safety of cryopreserved autologous bone flaps versus titanium plates for cranioplasty in patients with cranial defects. METHODS:Sixty patients with cranial defects admitted to our hospital from January 2021 to June 2024 were retrospectively selected. They were assigned to the autologous bone group (n = 30, cranioplasty with cryopreserved autologous bone flaps) and the titanium plate group (n = 30, cranioplasty with titanium plates) according to the reconstruction material. The perioperative indicators, outcome for cranioplasty, neurological function recovery, incidence of complications, and treatment costs were compared between the two groups. RESULTS:The autologous bone group exhibited significantly better outcomes for cranioplasty at 3 and 6 months postoperatively than the titanium plate group (p < 0.05). At 6 months postoperatively, the autologous bone group exhibited significantly higher NIHSS scores than the titanium plate group (p < 0.05). The intracranial pressure levels were significantly lower at all postoperative time points in the autologous bone group than in the titanium plate group (p < 0.05). The autologous bone group demonstrated faster recovery of inflammatory indicators, lower overall incidence of complications (6.67% vs. 30.00%) (χ2=4.588, p = 0.032), and lower hospitalization costs and material expenses than the titanium plate group (p < 0.05). CONCLUSION:Cryopreservation of autologous bone flaps for cranioplasty is associated with improved bone healing, better neurological recovery, reduced complication rates, and lower medical costs. However, these observational findings require further validation through prospective randomized controlled trials. Nevertheless, the current evidence supports the potential clinical application of this technique when feasible.
This study aimed to examine the effects of sericin on diabetic cognitive impairment (DCI) in rats based on neuroinflammation. SD rats were first fed with a high sugar and high fat diet for 4 weeks, and then injected with 50 mg/kg streptozotocin intraperitoneally to establish a diabetic model. The diabetic rats were randomly divided into 3 groups and treated with distilled water (n = 10), 500 mg/kg (n = 10) or 1000 mg/kg (n = 20) sericin, respectively, by gavage once a day for 8 weeks. Before the end of the trial, 10 rats in the 1000 mg/kg sericin group were injected with 10 μg EX527, a Sirtuin-1 (SIRT1) inhibitor, into the lateral ventricles once every other day for 5 times. Treated with sericin significantly reduced fasting blood glucose and improved DCI in rats. Sericin significantly inhibited neuroinflammation and microglial activation, reduced the expression of NOD-like receptor protein 3 (NLRP3) and thioredoxin-interacting protein (TXNIP) proteins, and reduced cell apoptosis, while increasing the expression of SIRT1 protein in the hippocampus of diabetic rats. After inhibiting SIRT1 with EX527, the above effect of sericin on DCI rats was weakened. These results indicated that sericin may block DCI progression in rats by inhibiting TXNIP/NLRP3 neuroinflammation and neuronal apoptosis through SIRT1.
Traumatic intracerebral hemorrhage (TICH) is a severe neurological emergency whose metabolic mechanisms remain largely unresolved. This study used serum metabolomics analysis to compare the metabolic profiles of TICH patients (n = 10) with non-TICH controls (n = 10). LC-MS/MS analysis identified a total of 3183 metabolites. The relative abundances of benzene and its derivatives, organic acids and their derivatives were significantly increased in the serum of ICH patients, while fatty acid, glycerophospholipid, and sphingomyelin metabolites were generally decreased. Multidimensional statistical methods were used to screen for significantly differentially expressed metabolites. Metabolite regulatory networks revealed the potential roles of amino acid metabolism, lipid metabolism (GP/SP/FA), and aromatic compounds (benzenes) in regulating TICH metabolism. Enrichment analysis revealed that these metabolites were highly enriched in lipid metabolism, amino acid metabolism, and neural signaling pathways, and were significantly associated with inflammatory drug pathways. The differentially expressed metabolites were further mapped to the Human Metabolite Database (HMDB) and subjected to metabolic-disease association analysis, suggesting that these metabolites may be closely related to the pathogenesis of TICH. ROC analysis demonstrated good diagnostic performance of five key metabolites in both discovery and validation cohorts (AUC > 0.70), with hypoxanthine and L-histidine showing the highest accuracy (AUC > 0.93). Correlation analysis indicated that key metabolites were associated with hematoma volume, NIHSS and GCS scores. In vitro experiments further confirmed that, under conditions of neuronal injury, the changes in these metabolites exhibit consistency. This study provides a theoretical basis for the development of potential biomarkers and precise intervention strategies.
OBJECTIVE:To evaluate the association of admission neutrophil-to-lymphocyte ratio (NLR) with functional outcomes, intracranial hemorrhage (ICH), and mortality in patients with acute ischemic stroke (AIS). METHODS:We searched PubMed, Scopus, Web of Science, Cochrane CENTRAL, and Embase from inception until December 17, 2024. Studies examining admission NLR as a predictor for functional outcomes, ICH, and mortality in AIS patients were included. A meta-analysis was performed using pooled odds ratios (ORs) with 95% confidence intervals (CIs). Subgroup analyses were conducted based on treatment modality, time of measurement, hemorrhage type, and ethnicity. Heterogeneity was assessed using I2 statistics, and publication bias was evaluated using Egger's test. RESULTS:Sixty observational studies (31,853 patients), including 59 cohort studies and one cross-sectional study, were included. Higher admission NLR was significantly associated with unfavorable functional outcomes (OR: 1.10, 95% CI: [1.07, 1.14]), ICH (OR: 1.06, 95% CI: [1.03, 1.09]), and mortality (OR: 1.06, 95% CI: [1.04, 1.08]). Subgroup analysis indicated that NLR was associated with poor outcomes in AIS patients receiving mechanical thrombectomy and intravenous thrombolysis. CONCLUSION:Admission NLR is significantly associated with unfavorable functional outcomes, ICH, and mortality in AIS patients. Its predictive value remained evident in the MT and Asian subgroups; however, the association with unfavorable functional outcomes was not significant in the non-Asian subgroup, and the association with mortality in the IVT subgroup was also not significant. Given its accessibility and cost-effectiveness, NLR holds promise as a routine biomarker for stroke prognosis.
BACKGROUND:Perioperative neurocognitive disorders (PNDs) encompass delayed neurocognitive recovery (dNCR; ≤30 days) and postoperative neurocognitive disorder (NCD; >30 days). While the HMGB1-TLR4/NF-κB axis drives acute neuroinflammation, temporal dynamics beyond the acute phase and distinct contributions of HMGB1 versus TLR4 to dNCR-to-NCD transition remain elusive. This study investigated whether glycyrrhizin attenuates sevoflurane-surgery-induced recognition memory deficit via HMGB1-TLR4 modulation. METHODS:Eight-month-old male C57BL/6J mice underwent right common carotid artery dissection under prolonged sevoflurane anesthesia (3%, 2 h) with or without glycyrrhizin pretreatment (30 mg/kg, i.p.; n = 15/group for batch 1, n = 7/group for batch 2). Cognitive function was assessed via open field, novel object recognition, Y-maze, and Morris water maze. Hippocampal neuroinflammation , HMGB1-TLR4-NF-κB signaling, synaptic proteins , and Nissl staining were evaluated at postoperative days 7 and 20. RESULTS:Prolonged sevoflurane exposure combined with surgery induced recognition memory impairment and reduced platform crossings, both attenuated by glycyrrhizin. While peripheral IL-6 normalized by day 7, hippocampal cytokines (IL-6, IL-1β, TNF-α) and glial activation persisted through day 20. HMGB1 was elevated at day 7 but normalized by day 20, whereas TLR4/NF-κB remained elevated at both time points; glycyrrhizin suppressed this cascade. Synaptic proteins were reduced and CA3/dentate gyrus exhibited Nissl staining reductions at days 7 and 20, protected by glycyrrhizin, whereas CA1 showed no significant alterations. CONCLUSIONS:These findings demonstrate temporal dissociation between HMGB1 normalization and sustained TLR4/NF-κB activation following sevoflurane-surgery in middle-aged mice. Prophylactic glycyrrhizin attenuates recognition memory deficits and suppresses hippocampal neuroinflammation, though mechanistic inferences remain speculative and require rigorous validation.
Aim: Stroke is considered as one of the most prevalent causes of death and disability for the humans, although it is preventable and treatable. Earlier stroke detection and treatment management helps in enhancing the clinical outcomes, thereby significantly minimizing the risk of disease. Thus, this work presents a sophisticated deep learning-based stroke prediction framework using the Magnetic Resonance Imaging (MRI) and provides specialized and flexible diagnostic guidance.Methods: The developed stroke detection system begins by collecting the required MR images in the benchmark sources. Further, the gathered MR images are fed to the stroke lesion segmentation using the developed Region Masked Attention-based Multi-Dilated Inception Unet++ (RMA-MIUnet++), which is accurately focus on stroke-affected regions. The segmented images are acquired as the outcomes from the proposed RMA-MIUnet++ model. These segmented images are further classified in the developed Efficient InceptionV3 with Novel Activation Function (EIV3-NAF)-based stroke classification model. Results: The experimental validation is performed on the developed system by comparing it with other conventional methods. When considering the batch size at 48, the accuracy of the proposed model for dataset 1 is 97% and dataset 2 is 93.26%.Conclusion: The results achieved by the developed EIV3-NAF model clearly show enriched performance in classifying the strokes.
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.
AIM:This study aimed to evaluate whether early Bobath-based neurorehabilitation improves motor and functional recovery in patients with acute ischemic stroke and moderate-to-severe hemiparesis after anterior-circulation mechanical thrombectomy. METHODS:We conducted a single-center retrospective propensity score-matched cohort study comparing early Bobath-based neurorehabilitation with conventional rehabilitation in AIS patients with moderate-to-severe hemiparesis after anterior-circulation mechanical thrombectomy. Patients aged ≥18 years initiated rehabilitation within 30 days after the procedure, and complete discharge and follow-up data were required for inclusion in the matched cohort. The primary outcome was change in Fugl-Meyer Assessment (FMA) motor score from baseline to discharge. Secondary outcomes included Modified Barthel Index (MBI), Modified Ashworth Scale (MAS), modified Rankin Scale (mRS), quality of life, and safety outcomes during 12-month follow-up. RESULTS:After matching, 206 patients (103 per group) were included. At discharge, the Bobath group showed greater improvement in motor function and daily living ability than the conventional group (adjusted mean difference: FMA 5.7 points, 95% CI 3.4-8.0; MBI 6.6 points, 95% CI 4.0-9.3; both p < 0.001). Improvements remained significant at 3 months but not at 12 months. Functional independence (mRS ≤2) at 3 months was more frequent in the Bobath group (82.5% vs 73.8%; p = 0.05). Complication rates were similar between groups. CONCLUSIONS:Early Bobath-based neurorehabilitation is associated with better short-term motor and functional recovery without increased adverse events after mechanical thrombectomy. The between-group differences attenuated by 12 months; therefore, further multicenter prospective studies are needed to confirm durability and long-term benefit.
AIM:This study aimed to evaluate the clinical value of upper limb rehabilitation robot-assisted training in stroke patients. METHODS:A total of 101 stroke patients were assigned to either conventional rehabilitation plus robot-assisted upper limb training (n = 50) or conventional rehabilitation alone (n = 51). The Fugl-Meyer Assessment of the Upper Extremity (FMA-UE), Modified Ashworth Scale for Upper Extremity (MAS-UE), Action Research Arm Test (ARAT), Functional Independence Measure (FIM) and quality-of-life outcomes were assessed. Oxygenated haemoglobin (HbO2) levels in the affected primary motor cortex (M1), premotor cortex (PMC) and supplementary motor area (SMA) were measured. RESULTS:After treatment, both groups showed improvements in FMA-UE, MAS-UE, ARAT and FIM scores, with no significant difference between the groups. Quality of life improved in both groups; however, the study group had significantly higher post-treatment scores in the environmental, physical, social and psychological domains than the control group (p = 0.000). After treatment, HbO2 levels in the affected M1, PMC and SMA increased in both groups, with the study group showing higher levels (p < 0.05). CONCLUSION:Upper limb rehabilitation robot-assisted training improved quality of life and cortical activation in stroke patients but showed no additional benefit in motor function compared with conventional rehabilitation.
