NeuroMolecular Medicine最新文献

{"title":"Gastrodin Protects Neuronal Cells Against Oxidative Stress Through miRNA-125b-5p/Mamdc2 Axis.","authors":"Lei Hu, Chao Lin, Renfu Li, Shouying Xu, Qiang Xu, Zihao An, Chao Tang","doi":"10.1007/s12017-025-08854-0","DOIUrl":"10.1007/s12017-025-08854-0","url":null,"abstract":"<p><p>Deregulated reactive oxygen species (ROS) levels trigger oxidative stress (OS) injury that is closely associated with the pathophysiology of various neurological disorders. Therefore, therapeutic efforts at oxidative events in the pathway of neuronal degeneration would be promisingly helpful for intervention and treatment of related diseases. Here, we report that gastrodin, the main bioactive constituent of Rhizoma Gastrodiae, protects the mouse hippocampal HT22 cells from OS caused by hydrogen peroxide (H₂O₂), including the increased cell viability, elevated Glutathione (GSH) levels, decreased Malondialdehyde (MDA) activity, and down-regulated ROS levels with restored cell morphology. Through RNA-sequencing (RNA-Seq) and multiple experiments, we screened the gene Mamdc2 that could be a potential regulating target of gastrodin. Mechanistically, gastrodin exerts its protective effects on neuronal cells from oxidative injury by suppressing miRNA-125b-5p, which increases its target Mamdc2 expression. Overexpression of miR-125b-5p mimics significantly attenuates the gastrodin-triggered protective effects against H₂O₂ in HT22 cells, including the decreased cell viability, down-regulated GSH activity, increased MDA activity, and up-regulated ROS production, compared to the gastrodin-administration with control miRNA group. However, these results could be effectively restored by the ectopic expression of Mamdc2, leading to the opposite outcomes to those of miR-125b-5p mimics-overexpression. Thus, the current study provides evidence that gastrodin has the potential for intervention and therapy of OS injury-associated neurological diseases in future.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"29"},"PeriodicalIF":3.9,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008797","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":"Adhesion-Related Pathways and Functional Polarization of Astrocytes in Traumatic Brain Injury: Insights from Single-cell RNA Sequencing.","authors":"Xiaoyan Liu, Ji Xia, Wenjing Shao, Xiaoming Li, Danfeng Yuan, Jingru Xie, Liang Zhang, Yuqian Tang, Hui Zhao, Pengfei Wu","doi":"10.1007/s12017-025-08858-w","DOIUrl":"10.1007/s12017-025-08858-w","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) induces profound functional heterogeneity in astrocytes, yet the regulatory mechanisms underlying this diversity remain poorly understood. In this study, we analyzed single-cell RNA sequencing data from the cortex and hippocampus of TBI mouse models to characterize astrocyte subtypes and their functional dynamics. We identified two major reactive subtypes: A1 astrocytes, enriched in inflammatory response, synaptic regulation, and neurodegenerative disease-related pathways; and A2 astrocytes, enriched in lipid metabolism, extracellular matrix (ECM) remodeling, and phagosome formation pathways. These functional differences were consistently observed across datasets with varying injury severities. Notably, adhesion-related pathways-including gap junctions, adherens junctions, and calcium-dependent adhesion-showed significant subtype-specific expression patterns and temporal shifts. Pseudotime trajectory analysis further suggested a potential transition between A1 and A2 states, accompanied by dynamic regulation of adhesion-related genes. Our findings highlight the complex and context-dependent roles of astrocytes in TBI and propose cell adhesion as a key modulator of astrocyte functional polarization.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"30"},"PeriodicalIF":3.9,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144064267","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":"Unraveling the Role of NeuroD2 in Ischemic Pathophysiology: Insight into Neuroprotection Mechanisms Associated with AKT Survival Kinase.","authors":"Busenur Bolat, Cigdem Bayraktaroglu, Zehra Degirmenci, Ecem Cerah, Mehmet Sali, Edanur Kolcu, Dila Nur Bars, Cemil Aydin, Fatima Abasova, Abdulla Alisoy, Hasan Ege Atali, Mustafa Caglar Beker, Ulkan Celik, Merve Beker","doi":"10.1007/s12017-025-08852-2","DOIUrl":"10.1007/s12017-025-08852-2","url":null,"abstract":"<p><p>NeuroD2 (ND2), a neuron-specific transcription factor, is essential in neural differentiation and neuroplasticity, yet its regulation under neuronal injury is barely uncovered. Effective treatment strategies for ischemic conditions require extensive knowledge of the signaling pathways and mechanisms underlying ischemic pathophysiology. This study aims to uncover the neuroprotective role of ND2 in ischemia and its interactions with critical signaling pathways implicated in recovery. An in vitro ischemic stroke model oxygen-glucose deprivation (OGD) method was applied to neuro-2A (N2a) cells with lentiviral ND2 (LvND2) overexpression. DNA fragmentation and cell survival assays indicated ND2's neuroprotective and anti-apoptotic effects under OGD conditions. Proteomic profiling and interaction analyses showed that LvND2 regulated the synthesis of cellular signaling, proliferation and cell adhesion-related proteins, such as MAPK3, Mki67, and NCAM. Additionally, a positive correlation was observed between ND2 expression and phosphorylated AKT levels. To investigate the interaction between ND2 and the PI3K/AKT signaling pathway, the pathway was pharmacologically inhibited with Wortmannin 30 min before OGD induction. After 8 h of OGD followed by 16 h of reperfusion, cell survival, DNA fragmentation, and Western blot analyses were performed. LvND2 administration alone increased cellular survival, whereas its combination with Wortmannin resulted in decreased cell survival. Additionally, LvND2 alone reduced the number of TUNEL-positive cells, while its combination with Wortmannin remains non-significant. These findings suggest that ND2 and AKT function in a coordinated manner within the PI3K/AKT survival pathway. ND2 may modulate AKT activity, highlighting its potential as a therapeutic target for addressing ischemic pathophysiology through molecular therapies.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"28"},"PeriodicalIF":3.9,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12003519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CaMKIIα-NpHR-Mediated Optogenetic Inhibition of DRG Glutamatergic Neurons by Flexible Optic Fiber Alleviates Chronic Neuropathic Pain.","authors":"Jaisan Islam, Md Taufiqur Rahman, Muhammad Ali, Elina Kc, Hyun Jik Lee, Sang Hwan Hyun, Young Seok Park","doi":"10.1007/s12017-025-08848-y","DOIUrl":"10.1007/s12017-025-08848-y","url":null,"abstract":"<p><p>Glutamatergic neurons of the dorsal root ganglion (DRGg) exert a significant effect on peripheral nociceptive signal transmission. However, assessing the explicit modulatory effect of DRGg during chronic neuropathic pain (CNP) with neuromodulation techniques remains largely unexplored. Therefore, we inhibited DRGg by optogenetic stimulation and examined whether it could alleviate CNP and associated anxiety-related behaviors in a chronic compressed DRG (CCD) rat model. The CCD pain model was established by inserting an L-shaped rod into the lumbar 5 (L5) intervertebral foramen, and either AAV2-CaMKIIα-eNpHR3.0-mCherry or AAV2-CaMKIIα-mCherry was injected into the L5 DRG. Flexible optic fibers were implanted to direct yellow light into the L5 DRG. Pain and anxiety-related behavioral responses were assessed using mechanical threshold, mechanical latency, thermal latency, and open field tests. In vivo single-unit extracellular recording from the DRG and ventral posterolateral (VPL) thalamus was performed. CNP and anxiety-related behavioral responses along with increased neural firing activity of the DRG and VPL thalamus were observed in CCD animals. Enhanced expression of nociception-influencing molecules was found in the DRG and spinal dorsal horn (SDH). In contrast during optogenetic stimulation, specific DRGg inhibition markedly alleviated the CNP responses and reduced the DRG and VPL thalamic neural hyperactivity in CCD animals. Inhibition of DRGg also reduced the active expression of nociceptive signal mediators in the DRG and SDH. Taken together, our findings suggest that CaMKIIα-NpHR-mediated optogenetic inhibition of DRGg can produce antinociceptive effects in CCD rats during peripheral nerve injury-induced CNP condition by altering peripheral nociceptive signal input in the spinothalamic tract.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"26"},"PeriodicalIF":3.9,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971997","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":"Neuropeptide Signaling in Glioblastoma: A Comprehensive Review of the Current State and Future Direction.","authors":"Shahid Afridi, Mohd Muzzammil, Intezar Ali, Mehdi H Shahi","doi":"10.1007/s12017-025-08849-x","DOIUrl":"10.1007/s12017-025-08849-x","url":null,"abstract":"<p><p>Glioblastoma multiforme (GBM) is a highly aggressive brain tumor characterized by complex pathophysiology and significant clinical challenges. Emerging research emphasizes the crucial role of neuropeptides in GBM and its influence on tumor progression, immune modulation, and therapy resistance. This review highlighted the importance of neuropeptides and their receptors in maintaining brain homeostasis and the glioblastoma tumor microenvironment. We discussed new therapeutic frontiers, including neuropeptide receptors as therapeutic targets, renin-angiotensin system, peptide receptor modulation, targeted cytotoxic analogs (such as Bombesin and Somatostatin), and advances in targeted radiotherapy. The review highlighted the potential of neuropeptide-based targeted therapies to improve GBM patient outcomes and suggests future research directions. This underscores the importance of targeting neuropeptide-related pathways for innovative therapeutic strategies in GBM, aiming to enhance patient prognosis and effective treatment.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"27"},"PeriodicalIF":3.9,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144046131","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":"Exploring NLRP3 Inhibition as a Key Modulator in Neonatal Hypoxic-Ischemic Brain Injury.","authors":"Khiany Mathias, Richard Simon Machado, Taise Cardoso, Beatriz Naspolini, Josiane Prophiro, Fabricia Petronilho","doi":"10.1007/s12017-025-08851-3","DOIUrl":"10.1007/s12017-025-08851-3","url":null,"abstract":"<p><p>Neonatal hypoxic-ischemic (HI) injury is a critical condition associated with significant acute brain damage and long-term neurological impairments. Growing evidence highlights the role of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, a key multiprotein complex driving neuroinflammation, in the progression of neonatal HI brain injury. Activation of the NLRP3 inflammasome triggers the release of pro-inflammatory cytokines, including interleukin-1 beta (IL-1β), which plays a pivotal role in exacerbating brain damage. This article examines current research to better understand the relationship between neonatal HI, NLRP3 inflammasome activation, and neuroinflammatory process. Furthermore, it emphasizes the therapeutic potential of targeting this pathway, proposing its modulation as a promising neuroprotective strategy to reduce neuroinflammation and improve outcomes in affected neonates.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"25"},"PeriodicalIF":3.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812015","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":"5-Repurposed Drug Candidates Identified in Motor Neurons and Muscle Tissues with Amyotrophic Lateral Sclerosis by Network Biology and Machine Learning Based on Gene Expression.","authors":"Kubra Temiz, Aytac Gul, Esra Gov","doi":"10.1007/s12017-025-08847-z","DOIUrl":"10.1007/s12017-025-08847-z","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that leads to motor neuron degeneration, muscle weakness, and respiratory failure. Despite ongoing research, effective treatments for ALS are limited. This study aimed to apply network biology and machine learning (ML) techniques to identify novel repurposed drug candidates for ALS. In this study, we conducted a meta-analysis using 4 transcriptome data in ALS patients (including motor neuron and muscle tissue) and healthy controls. Through this analysis, we uncovered common shared differentially expressed genes (DEGs) separately for motor neurons and muscle tissue. Using common DEGs as proxies, we identified two distinct clusters of highly clustered differential co-expressed cluster genes: the 'Muscle Tissue Cluster' for muscle tissue and the 'Motor Neuron Cluster' for motor neurons. We then evaluated the performance of the nodes of these two modules to distinguish between diseased and healthy states with ML algorithms: KNN, SVM, and Random Forest. Furthermore, we performed drug repurposing analysis and text-mining analyses, employing the nodes of clusters as drug targets to identify novel drug candidates for ALS. The potential impact of the drug candidates on the expression of cluster genes was predicted using linear regression, SVR, Random Forest, Gradient Boosting, and neural network algorithms. As a result, we identified five novel drug candidates for the treatment of ALS: Nilotinib, Trovafloxacin, Apratoxin A, Carboplatin, and Clinafloxacin. These findings highlight the potential of drug repurposing in ALS treatment and suggest that further validation through experimental studies could lead to new therapeutic avenues.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"24"},"PeriodicalIF":3.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11968496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Folic Acid Promotes Peripheral Nerve Injury Repair via Regulating DNM3-AKT Pathway Through Mediating Methionine Cycle Metabolism.","authors":"Weibo Kang, Yanli Zhang, Wei Cui, Hua Meng, Duo Zhang","doi":"10.1007/s12017-025-08845-1","DOIUrl":"10.1007/s12017-025-08845-1","url":null,"abstract":"<p><p>Emerging evidence suggests that folic acid (FA) supports nerve repair, but its beneficial effects in peripheral nerve injury (PNI) remains unclear. This study aims to investigate protective effects of FA against PNI and the underlying molecular mechanisms. High-performance liquid chromatography-tandem mass spectrometry was utilized for precise quantification of metabolites. A sciatic nerve crush injury model was established in rats, followed by assessments of cell proliferation, apoptosis, and motor function using CCK-8 assays, flow cytometry, and the balance beam test, respectively. Neuromorphological observations, electromyography, and ELISA were conducted to evaluate structural, electrophysiological, and biochemical parameters. In vitro, FA restored methionine cycle balance in Schwann cells and neurons disrupted by enzyme inhibition, improving cell viability, reducing apoptosis, and preserving cellular structure. In vivo, FA supplementation restored S-adenosylmethionine and homocysteine levels in a methionine metabolism disorder model and enhanced motor function, neural morphology, neuron survival, and electrophysiological recovery after PNI. Epigenetic analyses revealed that FA modulated DNA methylation and histone modifications of the DNM3 promoter, influencing gene expression. Furthermore, FA facilitated nerve repair via the DNM3-AKT pathway, regulating apoptosis, autophagy, and oxidative stress-related enzymes. These findings highlight FA's potential in promoting nerve repair through metabolic and epigenetic mechanisms.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"23"},"PeriodicalIF":3.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of G-Protein-Coupled Receptor Kinase 4 in Modulating Mitophagy and Oxidative Stress in Cerebral Ischemia-Reperfusion Injury.","authors":"Jian Wang, Diheng Gu, Ke Jin, Hualong Shen, Yaohua Qian","doi":"10.1007/s12017-025-08843-3","DOIUrl":"10.1007/s12017-025-08843-3","url":null,"abstract":"<p><p>Cerebral ischemia-reperfusion injury (CIRI) causes significant neuronal damage through oxidative stress, inflammation, and mitochondrial dysfunction. The G-protein-coupled receptor kinase 4 (GRK4) has been implicated in regulating stress responses in various tissues, but its role in ischemic brain injury remains unclear. In this study, we investigated the role of GRK4 in oxidative stress, inflammation, and mitophagy during CIRI using both in vivo and in vitro models. For the in vivo experiments, we employed the bilateral common carotid artery occlusion (BCCAO) model to induce ischemia-reperfusion injury. Our finding demonstrated that ischemic reperfusion significantly upregulated GRK4 expression in the brain, correlating with elevated levels of inflammatory cytokines and oxidative stress markers. In cultured cerebellar neurons subjected to oxygen-glucose deprivation (OGD), over-expression of GRK4 decreased cell viability, while GRK4 inhibition enhanced neuronal survival, suggesting that GRK4 exacerbates neuronal damage in ischemic conditions. Furthermore, GRK4 overexpression impaired mitophagy, as indicated by altered expression of key mitophagy-related proteins (Beclin-1, PINK1, and p62), which led to mitochondrial dysfunction and increased oxidative stress. In contrast, GRK4 inhibition promoted more efficient mitophagy and improved mitochondrial quality control. These results highlight the detrimental role of GRK4 in ischemic brain injury and suggest that targeting GRK4 could offer a novel therapeutic strategy to mitigate neuronal damage by balancing oxidative stress, inflammation, and mitochondrial dynamics. Further studies are needed to elucidate the precise molecular mechanisms underlying GRK4-mediated neuroinflammation and mitochondrial dysfunction in ischemic stroke.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"21"},"PeriodicalIF":3.9,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586395","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":"SP3-Mediated Transcriptional Activation of GRIK1 is Involved in Alzheimer's Disease-Induced Cognitive Decline by Inducing Inflammasome Activation in Microglia.","authors":"Xiaolin Pang, Zhun Wang, Mengxue Zhang, Jinpeng Dong, Zhonglan Dong, Yiqing Yin","doi":"10.1007/s12017-025-08844-2","DOIUrl":"10.1007/s12017-025-08844-2","url":null,"abstract":"<p><p>GRIK1 has been identified to suppress the activation of NLRP3 inflammasome. The present study investigated the damaging effect of GRIK1 on Alzheimer's disease (AD), the most common neurodegenerative disease, by focusing on inflammasome. APP-PS1 mice were subjected to a Y-maze test and a Morris water maze test. APP-PS1 mice with GRIK1 knockdown were constructed using adeno-associated virus, and the effects of GRIK1 knockdown on the NLRP3 inflammasome activation in microglia of brain tissues of APP-PS1 mice were analyzed. Mouse primary microglia BV2 was induced by LPS, and Western blot, flow cytometry, and ELISA were performed. GRIK1 was significantly elevated in the brain tissues of APP-PS1 mice. GRIK1 knockdown inhibited the neuronal damage and NLRP3 neuroinflammation in the brain tissues and improved cognitive dysfunction of APP-PS1 mice. Knockdown of GRIK1 inhibited activation of NLRP3 inflammasome in BV2 cells. SP3 was upregulated in the brain tissues of APP-PS1 mice, and SP3 promoted GRIK1 transcription by binding to its promoter. Overexpression of GRIK1 reversed the mitigating effect of knockdown of SP3 on cognitive dysfunction and NLRP3 activation in APP-PS1 mice. Overall, our results revealed that SP3-induced GRIK1 transcription potentiates NLRP3 inflammasome activation in microglia, leading to cognitive dysfunction in AD.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"27 1","pages":"22"},"PeriodicalIF":3.9,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586394","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}