The International Journal Of Neuroscience[JOURNAL]
Sun
200 papers
Vagus nerve stimulation ameliorates learning-memory deficits and suppresses neuronal apoptosis via the ERK/CREB/BDNF signaling pathway in epileptic rats.
Lu Y, Li Y, Su W … +4 more , Lv Y, Zheng Z, Zhao A, Wang Z
Int J Neurosci · 2026 Mar · PMID 40757650 · Publisher ↗
PURPOSE: This study aimed to evaluate the impact of vagus nerve stimulation (VNS) on learning, memory and neuronal apoptosis in epileptic rats, and to investigate the involvement of the ERK/CREB/BDNF signaling pathway. M...
PURPOSE: This study aimed to evaluate the impact of vagus nerve stimulation (VNS) on learning, memory and neuronal apoptosis in epileptic rats, and to investigate the involvement of the ERK/CREB/BDNF signaling pathway. METHODS: Epilepsy was induced in rats lithium chloride-pilocarpine. Then they were divided into four groups: epilepsy model, VNS-treated, and sodium valproate-treated (VPA), and sham groups ( = 6/group). VNS was administered at parameters of 1 mA, 30 Hz, 250 μs pulse width, for 30 min/12 h. Cognitive function was assessed by the Morris water maze. Hippocampal neuronal damage, apoptosis and pathology were evaluated Nissl, TUNEL and H&E staining, respectively. Oxidative stress markers were quantified by ELISA, while ROS were detected using DCFH-DA probes. Western blotting analyzed expression levels of Bcl-2, Bax, ERK, p-ERK, CREB, p-CREB and BDNF in the cerebral cortex. RESULTS: Healthy rats exhibited abundant, evenly distributed Nissl bodies and orderly arranged cortical neurons. The epilepsy group showed cytoplasmic hypochromia and disorganized neuronal arrangement. VNS restored neuronal morphology to an extent comparable with VPA treatment. Compared to sham group, the epilepsy group demonstrated increased seizure frequency, duration, Racine scores, and escape latency, alongside reduced target quadrant occupancy. Elevated MDA, TNF-α and ROS levels were observed in the cerebral cortex, while SOD, IL-10, p-ERK/ERK, p-CREB/CREB and BDNF levels were reduced. VNS significantly ameliorated these pathological changes. CONCLUSION: VNS enhances cognitive function in epileptic rats, potentially through activation of the ERK/CREB/BDNF pathway in the cerebral cortex, thereby attenuating oxidative stress and neuroinflammation.
A mitochondrial-derived peptide MOTS-c contributes to the protective effect against brain injury associated with LPS-induced sepsis by strengthening the blood-brain barrier's ultrastructure.
Bai Y, Wu H, Wang X … +4 more , Guo Y, Gong B, Dong B, Yu Y
Int J Neurosci · 2026 Mar · PMID 40753494 · Publisher ↗
BACKGROUND: Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis, increasing short-term and long-term mortality. It involves neuroinflammation, neuronal damage, and blood-brain barrier (BBB) disrupt...
BACKGROUND: Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis, increasing short-term and long-term mortality. It involves neuroinflammation, neuronal damage, and blood-brain barrier (BBB) disruption. MOTS-c, a mitochondrion-derived peptide, exerts neuroprotective effects by modulating inflammatory responses and cellular functions. This study explored the protective effects of MOTS-c against brain injury in mice with LPS-induced sepsis. METHODS: A mouse model of sepsis was established intraperitoneal injection of LPS. The mice were divided into four groups: Control, Control + MOTS-c, LPS, and LPS + MOTS-c groups. The mice in the latter two groups received MOTS-c (20 mg/kg) four hours before model establishment. Survival rates and the murine sepsis score (MSS) were recorded. H&E staining, ELISA, Evans blue staining, brain water content detremination, immunofluorescence staining, western blotting, and qPCR were performed to assess brain tissue damage, inflammation, BBB permeability, and BBB-related protein expression. RESULTS: MOTS-c treatment increased the survival rate, decreased the MSS score, alleviated brain tissue damage, downregulated the expression of inflammatory factors, reversed the increase in BBB permeability, upregulated the expression of BBB-related proteins and CD31/PDGFRβ, decreased the expression of GFAP/Iba-1/MMP-9, and increased the expression of neurotrophic factors in septic mice. CONCLUSION: MOTS-c effectively reduced mortality rates and the MSS, attenuated neuroinflammatory responses, mitigated increase in BBB permeability, promoted neurotrophic factor production, and protecting against brain injury in mice with LPS-induced sepsis.
Bilateral adduction palsy with a paramedian midbrain lesion is most likely wall-eyed bilateral oculomotor subnuclear ophthalmoplegia: a case report of a brainstem infarction.
Yasuda T, Fujiwara S, Shimomura A … +2 more , Chikada A, Arai N
Int J Neurosci · 2026 Mar · PMID 40650553 · Publisher ↗
A 73-year-old female was hospitalized in our Department of Neurology for diplopia due to multiple infarctions in the midbrain and pons. A neurological examination revealed bilateral adduction palsy during horizontal gaze...
A 73-year-old female was hospitalized in our Department of Neurology for diplopia due to multiple infarctions in the midbrain and pons. A neurological examination revealed bilateral adduction palsy during horizontal gaze with nystagmus of the contralateral abducting eye. Exotropia and impaired convergence were also noticed. The distinctive symptoms indicated wall-eyed bilateral internuclear ophthalmoplegia (WEBINO). We speculate that the cause of WEBINO in our case was bilateral medial rectus palsy bilateral damage to the medial rectus subnuclei (MRSN) due to the paramedian midbrain infarction. We propose that bilateral adduction palsy with impaired convergence due to bilateral MRSN impairment, such as in our case, should be given a more appropriate name because we speculate that it is not 'internuclear ophthalmoplegia'. 'WEBOSO' (wall-eyed bilateral oculomotor subnuclear ophthalmoplegia) may be a more appropriate name.
EEG signal analysis for the classification of Alzheimer's and frontotemporal dementia: a novel approach using artificial neural networks and cross-entropy techniques.
Latifoğlu F, Orhanbulucu F, Murugappan M … +3 more , Gürbüz SN, Çayır B, Avcı FZ
Int J Neurosci · 2026 Mar · PMID 40621732 · Publisher ↗
Dementia, a neurological disorder, can cause cognitive decline due to damage to the brain. Our study aims to contribute to the development of computer-aided diagnosis (CAD) systems to aid in the early diagnosis of Alzhei...
Dementia, a neurological disorder, can cause cognitive decline due to damage to the brain. Our study aims to contribute to the development of computer-aided diagnosis (CAD) systems to aid in the early diagnosis of Alzheimer's disease (AD) and frontotemporal dementia (FTD) by examining Electroencephalogram (EEG) signals. EEG signals of 36 AD, 23 FTD and 29 healthy control (HC) participants were analyzed and entropy measurement approaches were used to analyze the connectivity between EEG channel pairs. The cross-permutation entropy (CPE) method and the cross conditional entropy (CCE) method were analyzed separately and the fused cross entropy (FCE) method was also tested by combining these techniques to determine the most appropriate method for feature extraction from EEG signals. The features obtained from these techniques were then evaluated in the classification phase using two separate machine learning algorithms. According to the performance evaluation criteria, the FCE and artificial neural network (ANN) model showed the most successful performance in the classification of all groups. In terms of area under the curve (AUC) and accuracy rates, 99.85% AUC and 98.46% accuracy were obtained in AD&HC groups, 99.71% AUC and 98.10% accuracy in FTD&HC groups and 99.39% AUC, 96.61% accuracy in AD&FTD groups. With the same model, an AUC rate of 97.14% and accuracy rate of 73.86% was obtained for the classification of the triple group (AD&FTD&HC). It has been observed that the results of this study show successful performance compared to the results of similar studies.
A neuroeconomic theory of obsessive-compulsive disorder.
Kaçar AŞ, Moustafa AA, Hassan M … +2 more , Zeki M, Balcı F
Int J Neurosci · 2026 Feb · PMID 40611796 · Publisher ↗
While there are many studies on the neural bases of obsessive-compulsive disorder (OCD), there is a dire need for a neurocomputational framework to explain its symptoms. To this end, we use the Expected Value of Control...
While there are many studies on the neural bases of obsessive-compulsive disorder (OCD), there is a dire need for a neurocomputational framework to explain its symptoms. To this end, we use the Expected Value of Control (EVC) theory to conceptualize the information processing deficits underlying OCD. Specifically, we argue that when experiencing obsessions, weak cognitive control is favored due to the affective cost of disregarding anxiety-provoking obsessions (akin to ignoring a fire alarm). This affective cost leads to the overvaluation of the cost of cognitive control (deeming it expensive), favoring automatic responses in the form of compulsions. We also exercise other ways by which OCD symptoms can be explained within the same theoretical framework. We ground our EVC-based neuroeconomic account in different neural systems implicated in OCD, including the orbitofrontal cortex, dorsal anterior cingulate cortex (dACC), dorsolateral prefrontal cortex, and basal ganglia, which refer to different EVC constituents. Finally, we argue that input from the bed nucleus of the stria terminalis to dACC introduces the key affective cost information to the estimation of EVC.
Early imaging biomarker of MRI within 1-cm margin surrounding surgical cavity predicting the progression of lower grade gliomas: dual-centers experience.
Li W, Bai X, Cheng M … +1 more , Li Y
Int J Neurosci · 2026 Mar · PMID 40611776 · Publisher ↗
INTRODUCTION: More than 80% of postoperative tumor recurrences were within 1 cm of the postoperative tumor margin; therefore, characterizing the cavity microenvironment with a 1 cm margin was valuable for early warning o...
INTRODUCTION: More than 80% of postoperative tumor recurrences were within 1 cm of the postoperative tumor margin; therefore, characterizing the cavity microenvironment with a 1 cm margin was valuable for early warning of the progress after Lower grade gliomas (LGGs) surgery. AIM: To investigate the clinical utility of apparent diffusion coefficient (ADC) values within 1 cm of the postoperative tumor margin for predicting the postoperative progression of LGGs. METHODS: The clinical and imaging data of patients with glioma from the First Hospital of Qinhuangdao and Affiliated Hospital of ChengDe Medical College were collected as the training group and external validation group, respectively. The mean ADC value within 1 cm of the margins surrounding the surgical cavity was measured by two senior radiologists. Patients were divided into high- and low-risk subgroups based on the optimal ADC threshold determined using the X-tile software. Kaplan-Meier survival curves were constructed to capture the differences in progression-free survival (PFS) between the groups. The independent risk factors for PFS were determined using Cox proportional hazards models. RESULTS: The inter-observer agreement was significant for the max ADC (ICC = 0.902) and min ADC (ICC = 0.884). X-tile determined the optimal threshold of the training group to be 1345 × 10 mm/s, dividing patients into low-risk and high-risk groups. The high-risk group exhibited a significantly shorter PFS than that of the low-risk group. In the external validation group, poor prognosis in the low-risk group was significantly correlated with mADC. Univariate and multivariate Cox regression analyses indicated that the mADC was an independent risk factor for LGGs recurrence ( < 0.05). CONCLUSIONS: ADC values within 1-cm of the margin surrounding the residual cavity are risk factors for the first postoperative progression of LGGs, which should be added in routine postoperative surveillance protocols to predict the PFS of patients with LGG.
Causal associations between neuroinflammation-related genes and intracerebral hemorrhage: an integrated study of Mendelian Randomization and gene functional analysis.
Zhou Q, Wu S, Kang Y
Int J Neurosci · 2026 Feb · PMID 40601346 · Publisher ↗
AIM: Intracerebral hemorrhage (ICH) is a life-threatening stroke subtype where neuroinflammation plays a crucial role. However, the genetic basis for neuroinflammation in ICH remains unclear. METHODS: This study used Men...
AIM: Intracerebral hemorrhage (ICH) is a life-threatening stroke subtype where neuroinflammation plays a crucial role. However, the genetic basis for neuroinflammation in ICH remains unclear. METHODS: This study used Mendelian Randomization (MR) to investigate the causal impact of neuroinflammation-related genes on ICH risk. A two-sample MR analysis was conducted using genetic variants from large-scale genome-wide association studies (GWAS). The primary analytical methods included the inverse variance weighted (IVW) approach, supplemented by MR-Egger regression and the weighted median method. Protein-protein interaction (PPI) network analysis, Gene Ontology (GO) enrichment analysis, and Gene Set Enrichment Analysis (GSEA) were employed to explore the biological mechanisms underlying these associations. RESULTS: Elevated expression of the CHUK gene was significantly associated with increased ICH risk (OR = 1.17, 95% CI 1.02-1.35, = 0.0245 in the Ebi-ICH dataset; OR = 1.25, 95% CI 1.03-1.52, = 0.0252 in the Finn-ICH dataset). Similarly, the CTLA4 gene showed a strong association with ICH (OR = 1.29, 95% CI 1.10-1.52, < 0.01 in the Ebi-ICH dataset; OR = 1.23, 95% CI 1.02-1.47, = 0.0264 in the Finn-ICH dataset). These results suggest that these genes contribute to ICH through mechanisms involving the NF-κB signaling pathway and immune regulation. CONCLUSION: The findings reveal a significant genetic influence of CHUK and CTLA4 on ICH risk, provide potential targets for future therapeutic interventions, which could lead to the development of more effective treatment strategies for ICH.
Alterations in gut microbiota and plasma metabolites in patients with generalized anxiety disorder: a multi-omics study.
Li Y, Dai J, Wang M … +3 more , Yan C, Xiu M, Qu M
Int J Neurosci · 2026 Mar · PMID 40601331 · Publisher ↗
OBJECTIVE: Microecological and metabolic disorders of the gut may be involved in the pathogenesis of generalized anxiety disorder (GAD), but clinical multi-omics evidence of this is lacking. Our study aimed to investigat...
OBJECTIVE: Microecological and metabolic disorders of the gut may be involved in the pathogenesis of generalized anxiety disorder (GAD), but clinical multi-omics evidence of this is lacking. Our study aimed to investigate characteristic alterations in the gut microbiota and plasma metabolome of patients with GAD and evaluate their clinical diagnostic value. PATIENTS AND METHODS: Ninety subjects (60 patients with GAD and 30 healthy volunteers) were included. We employed 16S rRNA gene sequencing to characterize the gut microbiota and targeted liquid chromatography-mass spectrometry to analyze plasma metabolomic profiles. RESULTS: GAD was associated with increased abundances of , , and and decreased abundances of , , , and . Metabolomic analysis revealed 19 differential metabolites (upregulated in GAD: e.g. glutamic acid, cortisol; downregulated in GAD: e.g. γ-aminobutyric acid, serotonin). Enriched metabolic pathways included phenylalanine, tyrosine, and tryptophan biosynthesis; alanine, aspartate, and glutamate metabolism; and the biosynthesis of unsaturated fatty acids. Notably, microbiome-metabolome combined analysis revealed a significant correlation between intestinal flora disorders and changes in the plasma metabolic profile. The diagnostic model constructed based on the combined omics data exhibited excellent discriminatory efficacy, with areas under curve of 0.710, 0.986, and 0.997 for the microbiome, metabolome, and combined model, respectively. CONCLUSION: This study revealed the characteristic gut microbiome-plasma metabolome covariation pattern of GAD and identified biomarker combinations with potential diagnostic value. The identified biomarker group provides new insights into the gut-brain axis mechanism of GAD, providing important theoretical support for clarifying the pathogenesis of GAD and developing precise diagnosis strategies.
The effect of transcranial direct current stimulation (tDCS) and oxytocin on food craving and weight control in obese individuals with food addiction: a double-blind clinical trial.
Mehranpour A, Eskandari Z, Hejazi J … +2 more , Gazori T, Saboory E
Int J Neurosci · 2026 Feb · PMID 40544477 · Publisher ↗
BACKGROUND AND AIMS: Obesity has become a major public health burden worldwide due to the significant social and economic impacts of its associated comorbidities. Despite substantial advancements in obesity research, its...
BACKGROUND AND AIMS: Obesity has become a major public health burden worldwide due to the significant social and economic impacts of its associated comorbidities. Despite substantial advancements in obesity research, its prevalence continues to rise, and weight loss remains a persistent challenge despite numerous weight management programs. Food addiction has emerged as a novel factor contributing to obesity, garnering considerable attention. Some individuals consume specific foods in quantities exceeding their physiological needs, indicating a lack of control over their eating behavior. This study aimed to examine the possible synergistic effects of novel interventions (tDCS and oxytocin) on weight loss and food craving symptoms in obese individuals with food addiction. DESIGN: This randomized clinical trial study was conducted on obese individuals with food addiction. PARTICIPANTS: Sixty individuals of both genders with obesity (BMI ≥ 30). SETTING: Participants were selected through purposive sampling and randomly assigned to four groups (19 participants each). INTERVENTION(S): Oxytocin nasal spray, Transcranial Direct Current Stimulation (tDCS), combined oxytocin & tDCS, and sham groups treated for 15 days. MEASUREMENTS: Body weight and food craving symptoms before and after treatment. COMMENTS: All three experimental interventions significantly improved weight control and food craving symptoms. No significant difference was observed between the mean scores of the tDCS and oxytocin groups. However, the combined tDCS and oxytocin group demonstrated significant differences compared to the other three groups. It can be concluded that the simultaneous application of two therapeutic approaches has a synergistic effect and can be effectively utilized in treating individuals with food addiction.
Exploring the characteristics of retrograde trans-synaptic degeneration from retinal ganglion cells loss in patients with homonymous hemianopia caused by acquired cerebral lesions.
Wang F, Zhang H, Cao S … +4 more , Zhou H, Xu Q, Wei S, Peng C
Int J Neurosci · 2026 Feb · PMID 40503636 · Publisher ↗
AIM: The existence of retrograde trans-synaptic degeneration (RTD) had been a controversial due to no structural continuity of two neurons in human. The study aimed to detect the macular retinal ganglion cell layer (mRGC...
AIM: The existence of retrograde trans-synaptic degeneration (RTD) had been a controversial due to no structural continuity of two neurons in human. The study aimed to detect the macular retinal ganglion cell layer (mRGCL) loss in homonymous hemianopia (HH) patients caused by acquired cerebral lesions using optical coherence tomography (OCT) to explore RTD characteristics. METHODS: A total of 40 HH patients (80 eyes) were enrolled this study. All the patients underwent OCT examination to evaluate the peripapillary retinal nerve fiber layer (pRFNL) and mRGCL loss. Their VF defects (mean deviations [MDs]) were assessed by Humphrey Perimeter. RESULTS: pRNFL and mRGCL thicknesses in HH patients reduced markedly compared to that in healthy eyes. Temporal mRGCL thicknesses in ipsilateral eyes reduced 4.77 ± 7.98 μm ( = 0.002) in contrast to their contralateral eyes. Nasal mRGCL thickness in contralateral eyes reduced 5.75 ± 10.44 μm ( = 0.004), compared to their ipsilateral eyes. Additionally, trauma ( = 0.08) and tumor ( = 0.030) cerebral lesions caused more pRNFL loss than that of cerebrovascular diseases. VF defects (MD) had linear correlations to mRGCL thicknesses in nasal hemisphere in contralateral eyes ( = 0.397, = 0.0404). The mRGCL and pRNFL loss occurred as early as 2-3 months after cerebral lesions occurred and progressed over time. CONCLUSION: RTD caused by acquired cerebral lesions were objectively detected by OCT and its characteristics were consistent to anatomic features of visual pathway. The mRGCL loss due to RTD correlated to VF defects and trauma and tumors caused greater injuries in pRNFL. Visual pathway could be an ideal model and OCT is a useful tool for RTD.
Association of single nucleotide polymorphisms with Parkinson's disease: evidence from a case-control study.
Li T, Wang J, Gao G … +5 more , Tao B, Yu Q, Huang S, Zhang Y, Zhang P
Int J Neurosci · 2025 Oct · PMID 40389383 · Publisher ↗
BACKGROUND: A growing body of strong evidence shows that voltage-gated sodium channels genes play key roles in the development of sporadic Parkinson's disease (sPD). However, little data have been reported on the associa...
BACKGROUND: A growing body of strong evidence shows that voltage-gated sodium channels genes play key roles in the development of sporadic Parkinson's disease (sPD). However, little data have been reported on the association between single nucleotide polymorphisms (SNPs) and sPD. This study aimed to investigate the association between SCN2A gene polymorphisms and sPD. METHODS: 267 patients with sPD and 267 healthy controls were included in this study. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of in the serum of patients and healthy individuals. RESULTS: The distribution of the G allele of rs2304016 or the A allele of rs17183814 in was significantly higher in patients with sPD ( = 0.001). In subtype analysis, the frequency of the rs2304016 AG heterozygote significantly differed between the early onset PD (EOPD) and late-onset PD (LOPD) groups ( < 0.001). The frequency of the rs17183814 AG heterozygote was significantly higher in the male patients ( = 0.002). Furthermore, we found that the level of mRNA transcription in the serum of sPD patients was significantly lower than that in the control group ( < 0.05). The serum expression level of in patients with the AA genotype at rs17183814 was lower ( < 0.05). CONCLUSIONS: This study demonstrated a significant association between SNPs and the expression of with sPD. These findings contribute to a better understanding of the role of and SNPs in sPD.
Single-nucleus RNA sequencing of rostral ventromedial medulla in mice with trigeminal neuralgia.
Zhang X, Guo L, Lyu J … +4 more , Li X, Hao Y, Zhang Y, Bai X
Int J Neurosci · 2026 Feb · PMID 40315019 · Publisher ↗
To investigate the transcriptional changes and cell interactions following trigeminal neuralgia (TN) in different cell types in rostral ventromedial medulla (RVM). In this study, trigeminal neuropathic pain was induced i...
To investigate the transcriptional changes and cell interactions following trigeminal neuralgia (TN) in different cell types in rostral ventromedial medulla (RVM). In this study, trigeminal neuropathic pain was induced in mice by ligating the left infraorbital nerve. Ten days after nerve ligation, we performed single-nucleus RNA sequencing of the RVM cells from the Sham and TN groups. We identified neurons, astrocytes, microglial cells, oligodendrocytes, oligodendrocyte progenitor cells, Purkinje cells, neuroblasts, endothelial cells and fibroblasts in RVM tissue. After analyzing the cell-type-specific transcriptional changes in the RVM following nerve ligation, we found that the number of neurons and Purkinje cells in the RVM increased. Furthermore, the differentially expressed genes (DEGs) in neurons and astrocytes between the two groups was identified. The downregulated DEGs in neurons were significantly enriched in GABAergic synapse (such as and ). The upregulated DEGs in neurons were enriched in glutamatergic synapse and voltage-gated ion channels. The downregulated DEGs in astrocytes involved in regulation of the postsynaptic membrane and synaptic membrane were enriched. Notably, the CellChat analysis highlights the Slit2-Robo 1/2 signaling pathway as a key route of communication between neurons and astrocytes after nerve ligation. This study analyzed cell-type-specific transcriptional responses to pain, and identified the possible key genes involved in TN. We inferred cell-state-specific communication in various cell types. Our findings provide potential targets, such as Slit2-Robo 1/2, Gabrg3, Gabra2, Grm4, Grik2, Cadps2 and Camk4 on therapeutic strategies for neuropathic or orofacial pain.
Piezo1 is a pathogenic gene and therapeutic target for neurological diseases.
Wang H, Gou Z, Chen S … +1 more , Lu L
Int J Neurosci · 2026 Feb · PMID 40276938 · Publisher ↗
Piezo1 is a ubiquitously expressed non-selective cation channel protein found across various species. It possesses the ability to detect and respond to external mechanical forces, converting mechanical cues into intracel...
Piezo1 is a ubiquitously expressed non-selective cation channel protein found across various species. It possesses the ability to detect and respond to external mechanical forces, converting mechanical cues into intracellular bioelectrical events, thereby facilitating the propagation of electrochemical signals. Within the nervous system, Piezo1 is integral to synaptogenesis and myelination, modulation of pro-inflammatory mediators, neuropathic pain, cognitive processes, angiogenesis, and the regulation of cerebral hemodynamics, consequently impacting the pathogenesis and progression of neurological disorders. This review meticulously summarizes and synthesizes existing literature to provide an exhaustive overview of Piezo1's roles and mechanisms in a spectrum of neurological diseases, including neurodegenerative disorders, cerebrovascular accidents, traumatic brain injuries, gliomas, multiple sclerosis, and epilepsy. Additionally, it explores the potential therapeutic applications of targeting Piezo1. The discussion also encompasses the current research limitations, the imperative need for future investigations, and prospective strategies. Our analysis indicates that Piezo1 is a susceptibility gene for neurological conditions, and its expression inhibition may confer therapeutic benefits. In summary, this comprehensive review offers novel insights into the involvement of Piezo1 in neurological diseases and establishes a theoretical groundwork for the future development of Piezo1-targeted therapeutic interventions.
UCMSCs-derived exosomal SLIT2 alleviates ischemic stroke through the β-catenin/TCF4/USP20 signaling pathway.
Xiao R, Wang Q, Peng J … +3 more , Hu X, Chen M, Xia Y
Int J Neurosci · 2026 Feb · PMID 40272090 · Publisher ↗
BACKGROUND: Ischemic stroke (IS) is a disease that causes necrosis of brain tissues by inadequate blood supply to the brain. Umbilical cord mesenchymal stem cells (UCMSCs)-derived exosomes (UCMSCs-Exo) have been reported...
BACKGROUND: Ischemic stroke (IS) is a disease that causes necrosis of brain tissues by inadequate blood supply to the brain. Umbilical cord mesenchymal stem cells (UCMSCs)-derived exosomes (UCMSCs-Exo) have been reported to alleviate IS, and slit guidance ligand 2 (SLIT2) could promote neurological repair after IS. The aim of this research was to explore the potential mechanism of UCMSCs-derived exosomal SLIT2 on IS progression. METHODS: The middle cerebral artery occlusion (MCAO) rat and oxygen glucose deprivation/reperfusion (OGD/R)-induced cellular models were established, and then treated with UCMSCs-Exo. Cell viability and apoptosis were explored by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The expressions of ubiquitin specific peptidase 20 (USP20) and related apoptotic proteins were determined using Western blot. Immunofluorescence and immunohistochemistry were performed to evaluate the effect of SLIT2 on β-catenin nuclear translocation. The association between transcription factor 4 (TCF4) and promoter was investigated by chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assys. RESULTS: In the OGD/R-induced cell model, UCMSCs-derived exosomal SLIT2 increased cell viability, decreased apoptosis and promoted β-catenin nuclear translocation. Besides, β-catenin agonist (SKL2001) facilitated USP20 transcription by promoting TCF4 binding to promoter. Finally, TCF4 upregulated USP20 and inhibited OGD/R-induced cell damage. In the MCAO rat model, UCMSCs-derived exosomal SLIT2 mitigated IS by promoting β-catenin nuclear translocation, which activated the TCF4/USP20 pathway to inhibit apoptosis. CONCLUSION: UCMSCs-derived exosomal SLIT2 activated TCF4 by promoting β-catenin nuclear translocation, which transcriptionally upregulated USP20 expression, thereby attenuating OGD/R-induced neuroncell damage and ultimately leading to inhibition of IS progression.
Passive mapping of hand motor cortex across altered states of consciousness.
Tong Y, Fan Z, Zou X … +3 more , Yue Q, Wu Z, Chen L
Int J Neurosci · 2026 Feb · PMID 40260620 · Publisher ↗
OBJECTIVE: To evaluate the ability of median nerve stimulation (MNS)-induced high gamma band (HGB) activity in mapping the hand motor cortex at different states of consciousness. METHODS: Five patients undergoing awake c...
OBJECTIVE: To evaluate the ability of median nerve stimulation (MNS)-induced high gamma band (HGB) activity in mapping the hand motor cortex at different states of consciousness. METHODS: Five patients undergoing awake craniotomy were recruited. MNS-induced electrocorticographic signals were recorded from awake to anesthetic states, with the loss of consciousness (LOC) session divided into three stages (LOC1, LOC2, and LOC3) based on conscious level. HGB signals were analyzed to localize hand motor cortex. Linear models were applied to analyze HGB dynamics during LOC. RESULTS: The sensitivity of hand motor cortex mapping based on HGB average envelope at short-latency period was 100%, 96.67%±3.33%, 83.47%±8.19%, and 82.22%±11.44% for the awake, LOC1, LOC2 and LOC3 stages. The sensitivity for HGB average envelope at long-latency period was 92.67%±4.52%, 90.85%±4.13%, 72.27%±17.07%, and 40.53%±12.82% across the same stages. The sensitivity based on HGB average power at short-latency period decreased from 100% in awake stage to 72.83%±12.95%, 48.11%±15.95%, and 21.12%±5.70% across LOC stages. The sensitivity for HGB average power at long-latency period dropped from 92.67%±4.52% in awake stage to 70.94%±10.79%, 58.37%±17.49%, and 25.71%±14.95% in the subsequent LOC stages. The slope coefficient of the simple linear model for long-latency average envelope was significantly smaller than that for short-latency. In the linear mixed effects model, the Condition × Sliding Window estimate coefficient was -0.794. CONCLUSION: In awake state, HGB average envelope and average power both effectively localized hand motor cortex. With declining consciousness, the mapping ability of average power significantly deteriorated, while the mapping ability of short-latency average envelope remained relatively stable.
Early neurological bedside rehabilitation intervention on the recovery of activities of daily living in stroke patients.
Huang K, Li Y, Jie X … +2 more , Liu C, Jie H
Int J Neurosci · 2026 Feb · PMID 40230234 · Publisher ↗
BACKGROUND: Stroke is a common neurological disorder that leads to severe functional impairments and reduced quality of life. Early bedside rehabilitation plays a crucial role in recovery, but research on its effectivene...
BACKGROUND: Stroke is a common neurological disorder that leads to severe functional impairments and reduced quality of life. Early bedside rehabilitation plays a crucial role in recovery, but research on its effectiveness is limited. METHODS: This study aimed to assess the impact of early bedside rehabilitation on stroke patients. A total of 150 patients were randomly assigned to an intervention group ( = 75) and a control group ( = 75). The intervention group received physical therapy, occupational therapy, and speech therapy within 48 h of stroke onset. The control group received standard care. Assessments included activities of daily living (ADL), motor function, cognitive function, and quality of life. RESULTS: The intervention group showed significantly better outcomes in ADL, motor function, cognitive function, and quality of life compared to the control group. The intervention group had higher Barthel Index, modified Rankin Scale, Fugl-Meyer Assessment, Montreal Cognitive Assessment (MoCA), and Stroke-Specific Quality of Life Scale (SS-QOL) scores ( < 0.001). CONCLUSION: Early bedside rehabilitation in the neurology department significantly improves stroke patients' recovery, including ADL, motor function, cognitive function, and quality of life. These findings highlight the importance of early rehabilitation and a comprehensive, multidisciplinary approach in stroke care, which can improve recovery outcomes and overall quality of care.
Nomogram combined neuron-specific enolase and NIHSS for prediction of post stroke depression.
Yan C, Zheng W, Si T … +4 more , Huang L, Wen L, Shen H, Qu M
Int J Neurosci · 2026 Feb · PMID 40193139 · Publisher ↗
OBJECTIVE: The National Institutes of Health Stroke Scale (NIHSS) is a known risk factor for post-stroke depression (PSD). However, more objective indicators are needed. The role of neuron-specific enolase (NSE) in PSD d...
OBJECTIVE: The National Institutes of Health Stroke Scale (NIHSS) is a known risk factor for post-stroke depression (PSD). However, more objective indicators are needed. The role of neuron-specific enolase (NSE) in PSD development remains unclear. This study aimed to ascertain the correlation of NIHSS score and NSE with PSD risk, and establish a novel nomogram combining NSE and NIHSS for early PSD prediction. METHODS: A total of 172 patients with acute ischemic stroke (AIS) were involved. Baseline clinical data including NSE and NIHSS were collected. At 3-month follow-up, patients were categorized into PSD and non-PSD groups. Logistic models and restricted cubic spline curve were used to investigate the correlation between NIHSS, NSE and PSD. A corresponding nomogram was formulated. RESULTS: Among 172 patients with AIS, 63 (36.63%) were diagnosed with PSD, while 109 (63.37%) were non-PSD. The baseline NIHSS and NSE were positively correlated with the risk of 3-month PSD ( < 0.05). Multivariate logistic regression revealed that sex (OR= 2.168, 95% CI 1.038 ∼ 4.526), age (OR= 1.035, 95% CI 1.002 ∼ 1.070), NIHSS (OR= 1.164, 95% CI 1.022 ∼ 1.325) and NSE (OR= 1.180, 95% CI 1.037 ∼ 1.343) were independently associated with 3-month PSD (all < 0.05). The nomogram constructed using sex, age, baseline NIHSS score and NSE showed good discrimination, calibration, and clinical utility. CONCLUSION: NSE is a valuable tool for early identification of PSD risk. A combined prediction model incorporating NIHSS and NSE has been established for the personalized prevention and intervention of PSD.
Research progress on the application of virtual reality technology in patients with Duchenne muscular dystrophy.
Liu S, Wang X, Ren Y … +1 more , Peng L
Int J Neurosci · 2026 Feb · PMID 40189876 · Publisher ↗
Duchenne muscular dystrophy is a common hereditary muscular dystrophy, virtual reality technology as an emerging therapeutic method has been gradually applied to the rehabilitation treatment of Duchenne muscular dystroph...
Duchenne muscular dystrophy is a common hereditary muscular dystrophy, virtual reality technology as an emerging therapeutic method has been gradually applied to the rehabilitation treatment of Duchenne muscular dystrophy patients. This paper reviews the current management status of Duchenne muscular dystrophy patients, the application effect of virtual reality technology in the rehabilitation treatment of Duchenne muscular dystrophy patients, and points out the challenges faced by the application of virtual reality technology in the field of Duchenne muscular dystrophy, aiming to provide a basis for the care of muscular dystrophy patients.
Carbamazepine toxicity with concomitant levetiracetam therapy in patients with epilepsy.
Mishra A, Mishra BR, Mohapatra D … +3 more , Srinivasan A, Maiti R, Hota D
Int J Neurosci · 2026 Feb · PMID 40186593 · Publisher ↗
AIM: Drug interactions are crucial in understanding the efficacy and safety of co-administered antiepileptic drugs. This study aims to investigate drug interactions between carbamazepine (CBZ) and levetiracetam (LEV) and...
AIM: Drug interactions are crucial in understanding the efficacy and safety of co-administered antiepileptic drugs. This study aims to investigate drug interactions between carbamazepine (CBZ) and levetiracetam (LEV) and the factors associated with CBZ toxicity. METHODS: The present record-based case-control study analyzed data from 158 patients. A univariate analysis was done to identify the association of various factors with toxic trough CBZ concentrations. Frequentist disproportionality analysis was done to determine a signal for the association between concomitant LEV administration and CBZ toxicity. Receiver operating characteristic (ROC) analysis was done to identify the LEV:CBZ dose ratio to differentiate between toxic and non-toxic CBZ concentrations. RESULTS: The odds of developing manifestations of CBZ toxicity in CBZ + LEV CBZ group were 16.65 (95% confidence interval [CI]: 3.52-78.70; < 0.001). The univariate analysis showed no association between CBZ dose and toxic trough CBZ levels, while an association between LEV administration and toxic trough CBZ levels was evident. A reporting odds ratio (ROR) of 2.25 (95% CI: 1.07-4.72; = 0.030) and proportional reporting ratio (PRR) of 1.77(95% CI: 1.07-2.94) was observed for toxic levels of CBZ with co-administration of LEV. A LEV: CBZ dose ratio of 1.86 was identified as a threshold for differentiating between toxic and non-toxic serum concentrations with an accuracy of 72.9%. CONCLUSIONS: There is a temporal association between LEV administration and toxic blood levels and toxic symptoms of CBZ, the chances of which significantly higher when the dose ratio of LEV:CBZ is 1.86.
Investigating the therapeutic potential of naringin in MK-801-induced schizophrenia model: focus on cognitive impairment and miR-25-3p-regulated pathways.
Pu Y, Xu Y, Zhuo Z … +2 more , Xiao H, Xu X
Int J Neurosci · 2026 Jan · PMID 40083156 · Publisher ↗
AIM: The aim of this study was to assess the ameliorative effects of naringin (NR) on cognitive impairment in schizophrenia(SZ) from multiple perspectives using behavioral, histopathological and molecular biological appr...
AIM: The aim of this study was to assess the ameliorative effects of naringin (NR) on cognitive impairment in schizophrenia(SZ) from multiple perspectives using behavioral, histopathological and molecular biological approaches. MATERIALS AND METHODS: SZ models were established in rats acute intraperitoneal injection of MK-801 in all groups except the control group, which received saline. Cognitive function was assessed using the Morris water maze test 21 days after prophylactic NR administration. Subsequently, Serum interleukin-6 (IL-6) and homocysteine (HCY) levels were quantified using enzyme-linked immunosorbent assay (ELISA), and hippocampal neuronal and synaptic structures were observed microscopy. Molecular detection was performed using real-time reverse transcription polymerase chain reaction (RT-qPCR) and western blotting (WB) to assess the expression levels of molecules related to the microRNA-25-3p/salt inducible kinase 1/CREB regulated transcription coactivator 2/cAMP responsive element binding protein 1 (miR-25-3p/SIK1/CRTC2/CREB1) pathway, thereby elucidating the mechanism by which NR ameliorates cognitive impairment in SZ. RESULTS: NR was found to mitigate cognitive decline in learning and memory induced by MK-801. It lowered serum levels of IL-6 and HCY, reduced neuronal damage in the CA1 region of the hippocampus, increased the thickness of postsynaptic dense material, decreased the distance between synaptic gaps, decreased the expression of SIK1, and elevated the expression of miR-25-3p, CRTC2 and CREB1 in the hippocampus. CONCLUSION: NR may protect neurons in the CA1 region of the hippocampus and enhance synaptic plasticity by regulating the miR-25-3p/SIK1/CRTC2/CREB1 signaling pathway, thereby promoting cognitive improvement.
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