Neural Regeneration Research最新文献

{"title":"Adiponectin as a potential mediator of the pro-cognitive effects of physical exercise on Alzheimer's disease.","authors":"Hui-Hui Guo, Hai-Ning Ou, Jia-Sui Yu, Julia Macedo Rosa, Douglas Affonso Formolo, Tong Cheng, Suk-Yu Yau, Hector Wing Hong Tsang","doi":"10.4103/NRR.NRR-D-23-00943","DOIUrl":"10.4103/NRR.NRR-D-23-00943","url":null,"abstract":"<p><p>Alzheimer's disease is the primary cause of dementia and imposes a significant socioeconomic burden globally. Physical exercise, as an effective strategy for improving general health, has been largely reported for its effectiveness in slowing neurodegeneration and increasing brain functional plasticity, particularly in aging brains. However, the underlying mechanisms of exercise in cognitive aging remain largely unclear. Adiponectin, a cell-secreted protein hormone, has recently been found to regulate synaptic plasticity and mediate the antidepressant effects of physical exercise. Studies on the neuroprotective effects of adiponectin have revealed potential innovative treatments for Alzheimer's disease. Here, we reviewed the functions of adiponectin and its receptor in the brains of human and animal models of cognitive impairment. We summarized the role of adiponectin in Alzheimer's disease, focusing on its impact on energy metabolism, insulin resistance, and inflammation. We also discuss how exercise increases adiponectin secretion and its potential benefits for learning and memory. Finally, we highlight the latest research on chemical compounds that mimic exercise-enhanced secretion of adiponectin and its receptor in Alzheimer's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"96-106"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural functional rehabilitation: Exploring neuromuscular reconstruction technology advancements and challenges.","authors":"Chunxiao Tang, Ping Wang, Zhonghua Li, Shizhen Zhong, Lin Yang, Guanglin Li","doi":"10.4103/NRR.NRR-D-24-00613","DOIUrl":"10.4103/NRR.NRR-D-24-00613","url":null,"abstract":"<p><p>Neural machine interface technology is a pioneering approach that aims to address the complex challenges of neurological dysfunctions and disabilities resulting from conditions such as congenital disorders, traumatic injuries, and neurological diseases. Neural machine interface technology establishes direct connections with the brain or peripheral nervous system to restore impaired motor, sensory, and cognitive functions, significantly improving patients' quality of life. This review analyzes the chronological development and integration of various neural machine interface technologies, including regenerative peripheral nerve interfaces, targeted muscle and sensory reinnervation, agonist-antagonist myoneural interfaces, and brain-machine interfaces. Recent advancements in flexible electronics and bioengineering have led to the development of more biocompatible and high-resolution electrodes, which enhance the performance and longevity of neural machine interface technology. However, significant challenges remain, such as signal interference, fibrous tissue encapsulation, and the need for precise anatomical localization and reconstruction. The integration of advanced signal processing algorithms, particularly those utilizing artificial intelligence and machine learning, has the potential to improve the accuracy and reliability of neural signal interpretation, which will make neural machine interface technologies more intuitive and effective. These technologies have broad, impactful clinical applications, ranging from motor restoration and sensory feedback in prosthetics to neurological disorder treatment and neurorehabilitation. This review suggests that multidisciplinary collaboration will play a critical role in advancing neural machine interface technologies by combining insights from biomedical engineering, clinical surgery, and neuroengineering to develop more sophisticated and reliable interfaces. By addressing existing limitations and exploring new technological frontiers, neural machine interface technologies have the potential to revolutionize neuroprosthetics and neurorehabilitation, promising enhanced mobility, independence, and quality of life for individuals with neurological impairments. By leveraging detailed anatomical knowledge and integrating cutting-edge neuroengineering principles, researchers and clinicians can push the boundaries of what is possible and create increasingly sophisticated and long-lasting prosthetic devices that provide sustained benefits for users.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"173-186"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential treatment of Alzheimer's disease astrocyte pathology based on nuclear lipid regulation.","authors":"Masato Komai, Nobumasa Takasugi","doi":"10.4103/NRR.NRR-D-24-01125","DOIUrl":"10.4103/NRR.NRR-D-24-01125","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"322-323"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced neurogenesis after ischemic stroke: The interplay between endogenous and exogenous stem cells.","authors":"Ruxu Geng, Yuhe Wang, Renzhi Wang, Jun Wu, Xinjie Bao","doi":"10.4103/NRR.NRR-D-24-00879","DOIUrl":"10.4103/NRR.NRR-D-24-00879","url":null,"abstract":"<p><p>Ischemic stroke is a significant global health crisis, frequently resulting in disability or death, with limited therapeutic interventions available. Although various intrinsic reparative processes are initiated within the ischemic brain, these mechanisms are often insufficient to restore neuronal functionality. This has led to intensive investigation into the use of exogenous stem cells as a potential therapeutic option. This comprehensive review outlines the ontogeny and mechanisms of activation of endogenous neural stem cells within the adult brain following ischemic events, with focus on the impact of stem cell-based therapies on neural stem cells. Exogenous stem cells have been shown to enhance the proliferation of endogenous neural stem cells via direct cell-to-cell contact and through the secretion of growth factors and exosomes. Additionally, implanted stem cells may recruit host stem cells from their niches to the infarct area by establishing so-called \"biobridges.\" Furthermore, xenogeneic and allogeneic stem cells can modify the microenvironment of the infarcted brain tissue through immunomodulatory and angiogenic effects, thereby supporting endogenous neuroregeneration. Given the convergence of regulatory pathways between exogenous and endogenous stem cells and the necessity for a supportive microenvironment, we discuss three strategies to simultaneously enhance the therapeutic efficacy of both cell types. These approaches include: (1) co-administration of various growth factors and pharmacological agents alongside stem cell transplantation to reduce stem cell apoptosis; (2) synergistic administration of stem cells and their exosomes to amplify paracrine effects; and (3) integration of stem cells within hydrogels, which provide a protective scaffold for the implanted cells while facilitating the regeneration of neural tissue and the reconstitution of neural circuits. This comprehensive review highlights the interactions and shared regulatory mechanisms between endogenous neural stem cells and exogenously implanted stem cells and may offer new insights for improving the efficacy of stem cell-based therapies in the treatment of ischemic stroke.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"212-223"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spinal cord injury-associated disruption of the autonomic immune control: Does biological sex matter?","authors":"Sara Rito-Fernandes, António J Salgado, Nuno A Silva, Susana Monteiro","doi":"10.4103/NRR.NRR-D-24-01078","DOIUrl":"10.4103/NRR.NRR-D-24-01078","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"298-299"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Positive impact of indicaxanthin from Opuntia ficus-indica fruit on high-fat diet-induced neuronal damage and gut microbiota dysbiosis.","authors":"Simona Terzo, Antonella Amato, Pasquale Calvi, Marta Giardina, Domenico Nuzzo, Pasquale Picone, Antonio Palumbo-Piccionello, Sara Amata, Ilenia Concetta Giardina, Alessandro Massaro, Ignazio Restivo, Alessandro Attanzio, Luisa Tesoriere, Mario Allegra, Flavia Mulè","doi":"10.4103/NRR.NRR-D-23-02039","DOIUrl":"10.4103/NRR.NRR-D-23-02039","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202601000-00036/figure1/v/2025-06-09T151831Z/r/image-tiff Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxanthin. This study investigated the impact of indicaxanthin on neuronal damage and gut microbiota dysbiosis induced by a high-fat diet in mice. The mice were divided into three groups according to different diets: the negative control group was fed a standard diet; the high-fat diet group was fed a high-fat diet; and the high-fat diet + indicaxanthin group was fed a high-fat diet and received indicaxanthin orally (0.86 mg/kg per day) for 4 weeks. Brain apoptosis, redox status, inflammation, and the gut microbiota composition were compared among the different animal groups. The results demonstrated that indicaxanthin treatment reduced neuronal apoptosis by downregulating the expression of proapoptotic genes and increasing the expression of antiapoptotic genes. Indicaxanthin also markedly decreased the expression of neuroinflammatory proteins and genes and inhibited high-fat diet-induced neuronal oxidative stress by reducing reactive oxygen and nitrogen species, malondialdehyde, and nitric oxide levels. In addition, indicaxanthin treatment improved the microflora composition by increasing the abundance of healthy bacterial genera, known as producers of short-chain fatty acids ( Lachnospiraceae , Alloprovetella , and Lactobacillus ), and by reducing bacteria related to unhealthy profiles ( Blautia , Faecalibaculum , Romboutsia and Bilophila ). In conclusion, indicaxanthin has a positive effect on high-fat diet-induced neuronal damage and on the gut microbiota composition in obese mice.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"324-332"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Empowering the NSC-34 cell line as a motor neuron model: Cytosine arabinoside's action.","authors":"Giuseppe Vitale, Susanna Amadio, Francesco Liguori, Cinzia Volonté","doi":"10.4103/NRR.NRR-D-24-00034","DOIUrl":"10.4103/NRR.NRR-D-24-00034","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202601000-00039/figure1/v/2025-06-09T151831Z/r/image-tiff The NSC-34 cell line is a widely recognized motor neuron model and various neuronal differentiation protocols have been exploited. Under previously reported experimental conditions, only part of the cells resemble differentiated neurons; however, they do not exhibit extensive and time-prolonged neuritogenesis, and maintain their duplication capacity in culture. The aim of the present work was to facilitate long-term and more homogeneous neuronal differentiation in motor neuron-like NSC-34 cells. We found that the antimitotic drug cytosine arabinoside promoted robust and persistent neuronal differentiation in the entire cell population. Long and interconnecting neuronal processes with abundant growth cones were homogeneously induced and were durable for up to at least 6 weeks in culture. Moreover, cytosine arabinoside was permissive, dispensable, and mostly irreversible in priming NSC-34 cells for neurite initiation and regeneration after mechanical dislodgement. Finally, the expression of the cell proliferation antigen Ki67 was inhibited by cytosine arabinoside, whereas the expression levels of neuronal growth associated protein 43, vimentin, and motor neuron-specific p75, Islet2, homeobox 9 markers were upregulated, as confirmed by western blot and/or confocal immunofluorescence analysis. Overall, these findings support the use of NSC-34 cells as a motor neuron model for properly investigating neurodegenerative mechanisms and prospectively identifying neuroprotective strategies.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"357-364"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hidden face of Parkinson's disease: Is it a new autoimmune disease?","authors":"Min Gi Jo, Seon-Hee Kim, Seung Pil Yun","doi":"10.4103/NRR.NRR-D-24-01063","DOIUrl":"10.4103/NRR.NRR-D-24-01063","url":null,"abstract":"<p><p>Parkinson's disease is a neurodegenerative disorder marked by the degeneration of dopaminergic neurons and clinical symptoms such as tremors, rigidity, and slowed movements. A key feature of Parkinson's disease is the accumulation of misfolded α-synuclein, forming insoluble Lewy bodies in the substantia nigra pars compacta, which contributes to neurodegeneration. These α-synuclein aggregates may act as autoantigens, leading to T-cell-mediated neuroinflammation and contributing to dopaminergic cell death. Our perspective explores the hypothesis that Parkinson's disease may have an autoimmune component, highlighting research that connects peripheral immune responses with neurodegeneration. T cells derived from Parkinson's disease patients appear to have the potential to initiate an autoimmune response against α-synuclein and its modified peptides, possibly leading to the formation of neo-epitopes. Recent evidence associates Parkinson's disease with abnormal immune responses, as indicated by increased levels of immune cells, such as CD4 + and CD8 + T cells, observed in both patients and mouse models. The convergence of T cells filtration increasing major histocompatibility complex molecules, and the susceptibility of dopaminergic neurons supports the hypothesis that Parkinson's disease may exhibit autoimmune characteristics. Understanding the immune mechanisms involved in Parkinson's disease will be crucial for developing therapeutic strategies that target the autoimmune aspects of the disease. Novel approaches, including precision medicine based on major histocompatibility complex/human leukocyte antigen typing and early biomarker identification, could pave the way for immune-based treatments aimed at slowing or halting disease progression. This perspective explores the relationship between autoimmunity and Parkinson's disease, suggesting that further research could deepen understanding and offer new therapeutic avenues. In this paper, it is organized to provide a comprehensive perspective on the autoimmune aspects of Parkinson's disease. It investigates critical areas such as the autoimmune response observed in Parkinson's disease patients and the role of autoimmune mechanisms targeting α-synuclein in Parkinson's disease. The paper also examines the impact of CD4 + T cells, specifically Th1 and Th17, on neurons through in vitro and ex vivo studies. Additionally, it explores how α-synuclein influences glia-induced neuroinflammation in Parkinson's disease. The discussion extends to the clinical implications and therapeutic landscape, offering insights into potential treatments. Consequently, we aim to provide a comprehensive perspective on the autoimmune aspects of Parkinson's disease, incorporating both supportive and opposing views on its classification as an autoimmune disorder and exploring implications for clinical applications.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"57-61"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of epilepsy-related genes in a Drosophila model.","authors":"Xiaochong Qu, Xiaodan Lai, Mingfeng He, Jinyuan Zhang, Binbin Xiang, Chuqiao Liu, Ruina Huang, Yiwu Shi, Jingda Qiao","doi":"10.4103/NRR.NRR-D-24-00877","DOIUrl":"10.4103/NRR.NRR-D-24-00877","url":null,"abstract":"<p><p>Complex genetic architecture is the major cause of heterogeneity in epilepsy, which poses challenges for accurate diagnosis and precise treatment. A large number of epilepsy candidate genes have been identified from clinical studies, particularly with the widespread use of next-generation sequencing. Validating these candidate genes is emerging as a valuable yet challenging task. Drosophila serves as an ideal animal model for validating candidate genes associated with neurogenetic disorders such as epilepsy, due to its rapid reproduction rate, powerful genetic tools, and efficient use of ethological and electrophysiological assays. Here, we systematically summarize the advantageous techniques of the Drosophila model used to investigate epilepsy genes, including genetic tools for manipulating target gene expression, ethological assays for seizure-like behaviors, electrophysiological techniques, and functional imaging for recording neural activity. We then introduce several typical strategies for identifying epilepsy genes and provide new insights into gene‒gene interactions in epilepsy with polygenic causes. We summarize well-established precision medicine strategies for epilepsy and discuss prospective treatment options, including drug therapy and gene therapy for genetic epilepsy based on the Drosophila model. Finally, we also address genetic counseling and assisted reproductive technology as potential approaches for the prevention of genetic epilepsy.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"195-211"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the glymphatic system to promote α-synuclein clearance: a novel therapeutic strategy for Parkinson's disease.","authors":"Xiaoyue Lian, Zhenghao Liu, Zuobin Gan, Qingshan Yan, Luyao Tong, Linan Qiu, Yuntao Liu, Jiang-Fan Chen, Zhihui Li","doi":"10.4103/NRR.NRR-D-24-00764","DOIUrl":"10.4103/NRR.NRR-D-24-00764","url":null,"abstract":"<p><p>The excessive buildup of neurotoxic α-synuclein plays a pivotal role in the pathogenesis of Parkinson's disease, highlighting the urgent need for innovative therapeutic strategies to promote α-synuclein clearance, particularly given the current lack of disease-modifying treatments. The glymphatic system, a recently identified perivascular fluid transport network, is crucial for clearing neurotoxic proteins. This review aims to synthesize current knowledge on the role of the glymphatic system in α-synuclein clearance and its implications for the pathology of Parkinson's disease while emphasizing potential therapeutic strategies and areas for future research. The review begins with an overview of the glymphatic system and details its anatomical structure and physiological functions that facilitate cerebrospinal fluid circulation and waste clearance. It summarizes emerging evidence from neuroimaging and experimental studies that highlight the close correlation between the glymphatic system and clinical symptom severity in patients with Parkinson's disease, as well as the effect of glymphatic dysfunction on α-synuclein accumulation in Parkinson's disease models. Subsequently, the review summarizes the mechanisms of glymphatic system impairment in Parkinson's disease, including sleep disturbances, aquaporin-4 impairment, and mitochondrial dysfunction, all of which diminish glymphatic system efficiency. This creates a vicious cycle that exacerbates α-synuclein accumulation and worsens Parkinson's disease. The therapeutic perspectives section outlines strategies for enhancing glymphatic activity, such as improving sleep quality and pharmacologically targeting aquaporin-4 or its subcellular localization. Promising interventions include deep brain stimulation, melatonin supplementation, γ-aminobutyric acid modulation, and non-invasive methods (such as exercise and bright-light therapy), multisensory γ stimulation, and ultrasound therapy. Moreover, identifying neuroimaging biomarkers to assess glymphatic flow as an indicator of α-synuclein burden could refine Parkinson's disease diagnosis and track disease progression. In conclusion, the review highlights the critical role of the glymphatic system in α-synuclein clearance and its potential as a therapeutic target in Parkinson's disease. It advocates for further research to elucidate the specific mechanisms by which the glymphatic system clears misfolded α-synuclein and the development of imaging biomarkers to monitor glymphatic activity in patients with Parkinson's disease. Findings from this review suggest that enhancing glymphatic clearance is a promising strategy for reducing α-synuclein deposits and mitigating the progression of Parkinson's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"233-247"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}