Neuroprotection最新文献

{"title":"Comment on \"Vitamin E for intraventricular hemorrhage prevention in preterm neonates: A systematic review and meta-analysis\".","authors":"Prashant R Kokiwar, Ambreen S Chauhan, A Kavya, Archana Dhyani","doi":"10.1002/nep3.70029","DOIUrl":"10.1002/nep3.70029","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"4 2","pages":"188-189"},"PeriodicalIF":4.1,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13306104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders.","authors":"Jun Han Kuan, Roshan S Raghavan, Dawn Li Wei Koh, Wing Yeng Tan, Igor Iezhitsa, Renu Agarwal","doi":"10.1002/nep3.70026","DOIUrl":"10.1002/nep3.70026","url":null,"abstract":"<p><p>Neurodegenerative diseases such as Alzheimer's (AD), Parkinson's (PD), Huntington's (HD), and multiple sclerosis (MS) involve progressive neuronal loss driven by dysregulated neurotransmission, neuroinflammation, oxidative stress, and mitochondrial dysfunction. Cholesterol metabolism has emerged as a critical factor involved with both central and peripheral dysregulation contributing to pathology. This review synthesizes current evidence on cholesterol's role in neurodegeneration and evaluates the therapeutic potential of statins, which act via cholesterol-dependent and other pleiotropic mechanisms. A PubMed search covering 1985-2025 publications was conducted using terms related to neurodegenerative diseases, statins, cholesterol metabolism, neuroinflammation, oxidative stress, mitochondrial dysfunction, and neuroprotection. Studies were selected to highlight mechanistic insights into cholesterol regulation in the nervous system and clinical data on statin use. Neuronal loss in neurodegeneration is driven by processes including excitotoxicity, inflammation, and mitochondrial dysfunction. Excessive reactive oxygen species activate apoptotic pathways involving <i>BAX</i>, <i>BAK</i>, and <i>p53</i>. Dysregulated cholesterol metabolism is a significant contributor: In AD, the <i>ApoE</i> allele <i>ε4</i> (<i>ApoE4</i>) links elevated cholesterol to amyloid-β (Aβ) accumulation and cognitive decline; in PD, cholesterol shows mixed effects, with some studies suggesting protection and others linking high levels to α-synuclein aggregation and mitochondrial impairment. In HD reduced cholesterol biosynthesis correlates with neuronal loss, while MS associates with elevated cholesterol and cognitive dysfunction. Statins, widely used cholesterol-lowering agents, reduce Aβ production, enhance its clearance, and improve synaptic function. Beyond lipid lowering, they exert anti-inflammatory, antioxidant, and anti-apoptotic effects. Clinical outcomes remain mixed, with benefits influenced by statin type, dose, treatment duration, disease stage, and patient genetics. Statins show multifaceted neuroprotective potential through cholesterol-dependent and independent pathways. While preclinical data are encouraging, clinical evidence is heterogeneous. Long-term, stratified trials are needed to clarify efficacy, and tailoring therapy to disease-specific mechanisms may offer a viable strategy for mitigating neurodegeneration and enhancing neuronal survival.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"4 1","pages":"30-47"},"PeriodicalIF":4.1,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral in situ ischemic postconditioning: From bench to bedside and beyond.","authors":"Xiao Jiang, Wenbo Zhao, Yongbo Xu, Fanlei Meng, Ming Wei","doi":"10.1002/nep3.70024","DOIUrl":"10.1002/nep3.70024","url":null,"abstract":"<p><p>Ischemic postconditioning (IPostC) has emerged as a promising therapeutic strategy for mitigating ischemia-reperfusion injury in ischemic tissues. However, its neuroprotective potential following thrombectomy in acute ischemic stroke (AIS) remains underexplored in clinical settings. To address this gap, we conducted a review to evaluate the feasibility, clinical relevance, and safety of IPostC in AIS patients. This review is structured in four parts. First, we assess the translational success of IPostC from preclinical research to clinical applications in non-neurological organs. Second, we examine data from animal models of cerebral ischemia, including rodents and canines, to evaluate the potential applicability of IPostC in the brain. Based on an integrated synthesis of these findings, we argue that clinical translation of IPostC for stroke treatment is both feasible and potentially beneficial. Furthermore, by incorporating insights from related endovascular interventions, we refine the proposed IPostC protocol to support safer and more effective clinical implementation. Finally, we introduce a novel in situ neurointerventional IPostC technique and discuss its potential clinical implications.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"4 1","pages":"48-64"},"PeriodicalIF":4.1,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rehabilitation paired with vagus nerve stimulation for motor function of chronic ischemic stroke patients in China: Study protocol of a multicenter randomized controlled trial (Repair Study).","authors":"Anchao Yang, Yong Liu, Hongxing Huang, Xiaoqin Sun, Dawei Zang, Jun Lu, Qingping Tang, Yulian Zhu, Qi Yue, Weining Wang, Guohui Lu, Lang Shuai, Jun Wang, Yunqian Li, Li Bie, Zhenlan Li, Guoxing Xu, Jinghui Li, Tao Ding, Yanwu Guo, Wen Wu, Yuting Xu, Yuanxiang Lin, Zhiyong Wang, Fuxin Lin, Chunhua Hang, Rong Xu, Xiangyu Liu, Wenjun Hong, Kai Shu, Min Lu, Feng Hu, Ruobing Qian, Ming Wu, Liuzhong Sun, Min Wu, Yingchuan Chen, Qian Wang, Sihao Liu, Qiao Zhang, Shiyi Zuo, Binxia Zhang, Wei Wu, Zhongming Wang, Huayang Deng, Lijuan Quan, Renli Qi, Wei Wang, Fuchuan Huang, Xiemin Liang, Feng Wang, Yalan Wang, Zejian Chen, Jiang Ran, Liang Chen, Jianguo Zhang, Ying Mao","doi":"10.1002/nep3.70025","DOIUrl":"10.1002/nep3.70025","url":null,"abstract":"<p><strong>Background: </strong>Stroke remains the leading cause of long-term disability worldwide. Approximately 60% of individuals with chronic ischemic stroke experience persistent upper limb impairment that limits daily activities. The Repair Study aims to evaluate the safety and efficacy of vagus nerve stimulation (VNS) paired with rehabilitation in patients with chronic ischemic stroke in developing countries, including those with severe upper limb dysfunction, thereby generating evidence to support broader global application.</p><p><strong>Methods: </strong>It is a multicenter, triple-blinded, randomized controlled trial conducted across 13 centers in China. Up to 99 participants with upper limb motor impairment, 9 months to 10 years post-stroke, will be enrolled. All participants will undergo VNS implantation (Model G115R/G115, PINS Medical, Beijing, China) and be randomized 2:1 by a central randomization system to active stimulation (0.8 mA) or sham stimulation (0 mA) paired with standardized upper limb rehabilitation. The blinded phase includes 6 weeks of clinical therapy (three sessions/week, 90-120 min/session, ≥300 stimulation-movement repetitions) followed by 6 weeks of home-based therapy (30 min/day). Post-unblinding, the active VNS group continues home-based therapy, while the sham group receives 6 weeks of clinic-based therapy.</p><p><strong>Discussion: </strong>The primary outcome is the between-group difference in Fugl-Meyer Assessment for Upper Extremity scores at the end of 6 weeks of clinical therapy. Secondary outcomes include additional motor, functional, and quality-of-life measures. Safety will be assessed through adverse event monitoring. The Repair Study is a multicenter randomized controlled trial targeting chronic ischemic stroke populations in developing countries. It supplements the existing clinical evidence by enrolling patients with more servere motor dysfunction and being conducted in a developing country.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov: NCT06722677.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"4 1","pages":"80-93"},"PeriodicalIF":4.1,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory B cells in the central nervous system: From immune regulation to neuroprotection.","authors":"Luiza Stanaszek, Miroslaw Janowski","doi":"10.1002/nep3.70027","DOIUrl":"10.1002/nep3.70027","url":null,"abstract":"<p><p>This review examines the immunoregulatory functions of interleukin-10 (IL-10)-secreting regulatory B cells (Bregs), specifically focusing on their potential neuroprotective roles and therapeutic implications for central nervous system (CNS) disorders. We conducted a narrative review of the current literature to evaluate the defining characteristics, mechanisms of action, and functional significance of Bregs. We specifically analyzed their roles in modulating immune responses within the CNS following injury and in neurodegenerative contexts. Bregs are a distinct immunosuppressive B cell subset that operates primarily via IL-10 secretion. Their functions include suppressing pro-inflammatory cytokine production and directing T cell differentiation toward regulatory phenotypes. In CNS pathologies, evidence suggests that Bregs can infiltrate the blood-brain barrier following disruption. Once within the CNS, they exert neuroprotection and enhance neuronal survival, thereby mitigating post-injury inflammation. Bregs are essential to immune regulation with significant, although not fully elucidated, neuroprotective potential. Their ability to modulate CNS makes them viable therapeutic targets for the treatment of brain injuries and neurodegenerative diseases. However, clinical applications must consider the complexities of B-cell biology to avoid compromising immune homeostasis. Further research into Breg mechanisms is vital for developing safe, targeted therapies.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"4 1","pages":"4-13"},"PeriodicalIF":4.1,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A holistic view on disease-modifying aspects, comorbidities, and contemporary neuroprotective approaches.","authors":"Piotr Walczak, Shen Li, Xunming Ji, Johannes Boltze","doi":"10.1002/nep3.70023","DOIUrl":"10.1002/nep3.70023","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 4","pages":"299-302"},"PeriodicalIF":0.0,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12754563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of stem cells in pediatric neurology: Insights from clinical trials.","authors":"Daniel Bou Najm, Saada Alame","doi":"10.1002/nep3.70022","DOIUrl":"10.1002/nep3.70022","url":null,"abstract":"<p><p>Pediatric neurological disorders comprise diverse conditions that impair nervous system function in children and contribute substantially to global disease burden. Stem cell therapy has become a promising treatment in neurology due to the cells' ability to self-renew, ensuring a continuous supply of cells. Cells are harvested from various origins, notably embryonic tissues and adult sources such as bone marrow, adipose tissue, and umbilical cord. Therapeutic effects arise from cell or enzyme replacement, trophic support, immunomodulation, and paracrine actions of the secretome. This review summarizes clinical applications of stem cell therapies across pediatric neurological diseases-including autism spectrum disorder, cerebral palsy, traumatic brain and spinal cord injury, epilepsy, neuromuscular disorders, and lysosomal storage diseases-and appraises evidence from preliminary descriptive studies that update the field and reveal methodological limitations. Reported therapeutic effect differs markedly by cell type, disease biology, timing of intervention, dose, and delivery method, producing inconsistent clinical results. Positive functional or developmental improvements have been documented in selected reports, but safety concerns, heterogeneity in study design, short follow-up, and variable potency assays limit conclusions. Because stem cell populations share phenotypic features but vary in therapeutic capacity, a universal, one-size-fits-all strategy is unlikely to succeed. Critical gaps remain regarding long-term safety, durability, standardized manufacturing, and optimal clinical endpoints. Continued rigorous translational research, standardized clinical trials, and expanded long-term surveillance are essential to optimize these therapies and improve outcomes for affected children and to ensure equitable access for diverse pediatric populations worldwide and sustainable implementation.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 4","pages":"303-321"},"PeriodicalIF":4.1,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12754568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bibliometric analysis and core target identification of network pharmacology on neuroinflammation in central nervous system disorders: Trends, collaborations, and future directions.","authors":"Yifeng Zhang, Shuai Hou, Jian Li, Weihua Wang, Shuai Jia, Xiaolu Wang, Yulei Xia, Yanqiang Wang","doi":"10.1002/nep3.70019","DOIUrl":"10.1002/nep3.70019","url":null,"abstract":"<p><p>Neuroinflammation is increasingly recognized as a critical driver of central nervous system (CNS) disorders, and network pharmacology has emerged as a promising approach to elucidate its complex mechanisms and therapeutic strategies. This study provides a comprehensive bibliometric and scientometric analysis of publications over the past 13 years to characterize research trends, identify key contributors, and uncover core therapeutic targets in this field. Articles published between January 2012 and May 2024 were retrieved from the Web of Science Core Collection. Visualization and quantitative analyses were performed using CiteSpace (version 6.3.R1, Drexel University, PA, United States) and VOSviewer (version 1.6.20, Leiden University - CWTS, Netherlands) followed by network interaction analysis to identify central targets implicated in neuroinflammation. A total of 156 publications were analyzed, with the United States, China, and Germany leading global output. Beijing University of Chinese Medicine, Case Western Reserve University, and University System of Ohio were identified as the most influential institutions. <i>Nucleic Acids Research</i> was the most frequently cited journal, whereas <i>Journal of Ethnopharmacology</i> contributed the largest number of publications. Co-occurrence clustering revealed 13 thematic research areas, highlighting apoptosis, Panax notoginseng, dihydrochalcones, and quercetin as representative hotspots. Target interaction analysis identified signal transducer and activator of transcription 3 (<i>STAT3</i>), jun proto-oncogene (<i>JUN</i>), <i>AKT</i> serine/threonine kinase 1 (<i>AKT1</i>), tumor protein 53 (<i>TP53</i>), and interleukin-6 (<i>IL6</i>) as core molecular targets. The findings delineate a dynamic and evolving research landscape in this domain and clarify its organization around several pivotal molecular targets. The field is shifting away from the conventional \"one drug, one target\" paradigm toward multi-target therapeutic strategies, reflecting the multifactorial nature of neuroinflammation in CNS disorders. These insights highlight key molecular nodes and research directions, providing a foundation for precision medicine approaches and innovative drug development to improve treatment outcomes in neuroinflammatory CNS diseases.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 4","pages":"336-352"},"PeriodicalIF":4.1,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12754577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological relationship between Parkinson's disease and gallstone disease.","authors":"Chao Jiang, Jingying Ma, Jingyu Mu, Yuanyuan Fu, Yan Zhao, Yiming You, Zhiqiang Cui, Chuang Guo","doi":"10.1002/nep3.70021","DOIUrl":"10.1002/nep3.70021","url":null,"abstract":"<p><p>Compelling evidence indicates a significant connection between dysfunction of the gastrointestinal tract, the gut microbiome, and Parkinson's disease (PD), which aligns with the notion of the \"gut-brain axis\". While the exact mechanisms involved in gut-brain interactions are still not fully understood, the high incidence of gastrointestinal symptoms during the early stages of PD aids in the development of diagnostic biomarkers and prospective disease-modifying therapies. Importantly, a number of studies have revealed a possible association between gallstone disease (GD) and PD; nevertheless, the exploration of diverse risk factors and the theory suggesting that the onset of PD might be associated with GD requires further investigation. This review aims to explore the evidence that connects alterations in GD with PD, emphasizing mechanisms that promote gut dysbiosis, the gut-brain connection, changes in lipid profiles, genetic and dietary influences, as well as neuroinflammation. Furthermore, we assess the potential implementation of innovative therapeutic strategies, including probiotic treatments and gut microbiota transplantation, in patients with PD. Although the evidence supports an association between PD and GD, causality remains to be established. Prospective cohort studies are needed to determine whether gallstones represent a prodromal marker or a causal risk factor for PD, and to validate these pathways as novel diagnostic and therapeutic targets for PD.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 4","pages":"322-335"},"PeriodicalIF":4.1,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12754581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spinal cord transection repair occurs when Nestin+ cells differentiate into neurons within a taxol-collagen-enhanced microenvironment in mice.","authors":"Caixia Fan, He Jiang, Junyan Yan, Lifang Jin, Guoquan Fu, Weiwei Xue, Lulu Zhang","doi":"10.1002/nep3.70016","DOIUrl":"10.1002/nep3.70016","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Previous studies have shown that taxol promotes axon regeneration in nerve repair, but fails to bridge the two ends of a completely transected spinal cord. Our prior in vitro research revealed that taxol, a microtubule-stabilizing agent, promotes neural stem cells (NSCs) differentiation into neurons while inhibiting astrocyte differentiation. In vivo studies further demonstrated that taxol-scaffold enhances functional recovery in animals with complete spinal cord injury (SCI). This study aims to directly validate the role of taxol-collagen in guiding NSCs to differentiate into neurons at the SCI lesion site and clarify its molecular mechanism.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This study is an interventional experimental research based on animal models. The research objects are 8-week-old Nestin-CreER:tdTomato transgenic mice, as well as endogenous NSCs and spinal cord tissues at the SCI site. A total of 30 mice were used, divided into a control group (15 mice, injected with collagen gel) and an intervention group (15 mice, injected with collagen gel containing 256 ng taxol). Five mice from each group were sampled for detection at 2, 4, and 8 weeks, respectively. Mice with qualified genotypes, successful model establishment, and positive red fluorescent protein (RFP) labeling were included, while those that did not meet these criteria were excluded. The outcomes included indicators related to NSC differentiation, microenvironment, neural circuit, molecules, and functions. GraphPad Prism 8 (Prism 8.4.3.686, CA, USA) was used for normality test and unpaired &lt;i&gt;t&lt;/i&gt;-test (&lt;i&gt;α&lt;/i&gt; = 0.05).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Taxol-collagen was found to guide NSCs toward neuronal differentiation by remodeling the SCI microenvironment: at 2 weeks post-SCI, the co-localization of its RFP-labeled NSCs with doublecortin was higher versus control; at 4 weeks, the co-localization of RFP-labeled NSCs with beta-tubulin III was more versus control; at 8 weeks, chondroitin sulfate proteoglycan deposition at the injury site was less. It formed a nerve bridge to reconnect the rostral-caudal injury ends and improved functional recovery in animals with complete SCI, as at 8 weeks postsurgery, motor evoked potentials latency was shortened and amplitude difference increased compared with the control group (&lt;i&gt;n&lt;/i&gt; &gt; 6, all &lt;i&gt;p&lt;/i&gt; &lt; 0.05). RNA-sequencing further elucidated the molecular mechanism, showing 992 upregulated and 220 downregulated genes in the taxol-collagen group; quantitative polymerase chain reaction validated related genes (e.g., Hes1, &lt;i&gt;p&lt;/i&gt; &lt; 0.05); Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated those genes were enriched in Wingless/Int-1 and mechanistic target of rapamycin pathways.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;These findings provide theoretical support for the clinical application of taxol-collagen in SCI treatment. By promoting neuronal differentiation of NSCs at the injury site and el","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 4","pages":"358-369"},"PeriodicalIF":4.1,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12754570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}