Frontiers in Cellular Neuroscience最新文献

{"title":"From cellular diversity to coordinating nervous system function: the next frontier in non-neuronal cell biology.","authors":"Jason R Plemel","doi":"10.3389/fncel.2026.1934284","DOIUrl":"10.3389/fncel.2026.1934284","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1934284"},"PeriodicalIF":4.4,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13457066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skin innervation and its <i>in vitro</i> modeling.","authors":"Émilie Genin, Lucile Guerber, Elodie Aymard, Jacques Leng, Joëlle Amédée, Alexis Desmoulière, François Berthod","doi":"10.3389/fncel.2026.1904623","DOIUrl":"10.3389/fncel.2026.1904623","url":null,"abstract":"<p><p>Skin innervation consists of myelinated Aβ fibers connected to sensory corpuscles and responsible for the sense of touch, and of free nerve endings including myelinated Aδ fibers and unmyelinated C fibers, that detect temperature and transmit pain signals, in addition to induce neurogenic inflammation through the release of neuropeptides. Moreover, the ability of skin innervation to detect pathogens that trigger or modulate immune reactions, such as TH1, TH2, or TH17 responses, has recently been identified, further growing interest in studying these neuroimmune interactions in the context of skin diseases. To this end, increasing efforts are being devoted to the development of <i>in vitro</i> models capable of reproducing the interactions between skin innervation and the various cutaneous cell types in both 2D and 3D culture systems. Combining sensory neurons and Schwann cells in a skin model that must be maintained at the air-liquid interface to promote epidermal differentiation is complex. Furthermore, guiding the migration of neurites through the dermis to make contact with keratinocytes remains a major challenge. The most advanced tissue-engineered 3D models can reproduce innervated skin containing vascular networks and immune cells, while also recapitulating disease phenotypes with cells obtained from patients. Moreover, these models enable real-time monitoring of neuronal electrical activity by connecting neurons with microelectrode arrays. <i>In vitro</i> modeling of skin innervation and reproducing the phenotype of skin diseases, should enable major advances in the development of new therapies targeting innervation, with the key advantage to induce far fewer side effects than conventional anti-inflammatory treatments.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1904623"},"PeriodicalIF":4.4,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13457020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential effects of environmental enrichment and physical exercise on glial biology in aging and aging-related conditions: a systematic review.","authors":"Gaurav Singhal, Bernhard T Baune","doi":"10.3389/fncel.2026.1859424","DOIUrl":"10.3389/fncel.2026.1859424","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Aging is associated with progressive changes in glial cell dynamics, including altered morphology, activation states, and neuroimmune interactions of microglia, astrocytes, and other glial populations. These changes contribute to chronic neuroinflammation, impaired brain homeostasis, and increased vulnerability to cognitive decline and neurodegenerative disorders. Non-pharmacological lifestyle interventions such as environmental enrichment (EE) and physical exercise (PE) have shown promise in modulating brain aging, but their comparative and combined effects on glial cells remain incompletely understood.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;This systematic review aimed to synthesize and compare the effects of EE, PE, and their combination on glial cell dynamics during aging. Specific aims included evaluating their individual and combined impacts on microglial and astrocytic morphology and function, identifying molecular mechanisms and neuroimmune crosstalk, benchmarking experimental paradigms, and examining regional, temporal, and lifespan variations in outcomes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A systematic search was conducted in PubMed, Scopus, and Google Scholar up to November 2025, following PRISMA 2020 guidelines. Preclinical (primarily rodent) studies were included if they examined well defined EE (cognitive, sensory, and social stimulation), isolated PE, or combined interventions in physiological aging models or in disease, injury, or stress paradigms considered relevant to aging because they shared glial mechanisms such as chronic neuroinflammation or impaired cellular homeostasis. These model classes were interpreted separately during synthesis, and studies were required to report glial relevant outcomes. A structured risk-of-bias assessment using the SYRCLE tool was conducted. Data were narratively synthesized due to anticipated heterogeneity.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Included studies showed that EE is consistently associated with increase in microglial number and morphological complexity and modulates peripheral T cell subsets, with stronger effects observed after long-term exposure. In contrast, PE more consistently reverses age-related microglial gene expression changes and induces region-specific remodeling of astrocytic morphology. Combined EE+PE interventions produced additive benefits on neurogenesis but yielded variable and non-superior effects on glial modulation. Molecular pathways such as BDNF-TrkB signaling and inflammatory cascades mediated these effects, with neuroimmune crosstalk (particularly involving peripheral T cells) influencing central glial states. Methodological heterogeneity and limited sex-specific analyses constrained generalizability.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Environmental enrichment and PE exert distinct yet partially overlapping effects on glial plasticity and neuroinflammation across physiological aging and aging relevant pathological contexts, with EE showing","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1859424"},"PeriodicalIF":4.4,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13457000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRG1β-overexpressing mesenchymal stem cell-derived exosomes alleviate oxygen-glucose deprivation-mediated neuronal injury via the miR-296-3p/MAOA axis.","authors":"Kuihua Wang, Haizhen Xu, Xiaohui Ji, Shengjie Zhu, YanJun Lin, Hua Chen, Xiangping Chen, Xuyang Jiang, He Zhou, Jianxin Ye, Xiaoping Cui","doi":"10.3389/fncel.2026.1809758","DOIUrl":"10.3389/fncel.2026.1809758","url":null,"abstract":"<p><strong>Background: </strong>Cerebral ischemic injury is a severe neurological disorder necessitating effective therapeutic strategies. Neuregulin-1β (NRG1β) and microRNAs are critical for neuroprotection, but the mechanisms by which NRG1β regulates microRNAs in neuronal injury are not fully understood.</p><p><strong>Methods: </strong>We characterized mesenchymal stem cells (MSCs) through their phenotypic markers and multilineage differentiation potential, confirming NRG1β overexpression in engineered MSCs. Transmission electron microscopy and nanoparticle tracking analysis were used to isolate and characterize exosomes. <i>In vitro</i> studies evaluated the effects of MSC/NRG1β-exosomes on OGD-treated HT-22 neuronal cells.</p><p><strong>Results: </strong>Mesenchymal stem cells/NRG1β-exosomes significantly enhanced HT-22 neuronal survival while reducing apoptosis and reactive oxygen species (ROS). The treatment reduced oxidative stress by lowering malondialdehyde (MDA) levels and boosting superoxide dismutase (SOD) activity. It also inhibited inflammatory cytokines such as IL-1β, TNF-α, and IL-6. Studies conducted <i>in vivo</i> with a middle cerebral artery occlusion model demonstrated that MSC/NRG1β-exosomes led to a reduction in infarct size, enhanced histopathological results 24 h after injury. Mechanistically, these exosomes were enriched with miR-296-3p, targeting monoamine oxidase A (MAOA) for downregulation. Inhibition of miR-296-3p or MAOA overexpression negated the protective effects of MSC/NRG1β-exosomes.</p><p><strong>Conclusion: </strong>Our findings demonstrate that exosomes derived from NRG1β-overexpressing mesenchymal stem cells (MSCs) exert neuroprotective effects against ischemic injury by upregulating miR-296-3p. This microRNA targets MAOA, leading to a reduction in apoptosis, oxidative stress, and inflammation. These results highlight the therapeutic potential of MSC/NRG1β-exosomes and the miR-296-3p/MAOA signaling axis in the treatment of ischemic brain injury.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1809758"},"PeriodicalIF":4.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of astrocytes in spatial cognition, action and Alzheimer's disease.","authors":"Marion Gaborit, Anahita Arabi, Letizia Mariotti","doi":"10.3389/fncel.2026.1811370","DOIUrl":"10.3389/fncel.2026.1811370","url":null,"abstract":"<p><p>Astrocytes sense synaptic activity, neuromodulation, and metabolic signals, and respond by modulating neurotransmission, excitability, and plasticity in neural networks. Increasing evidence demonstrates that these processes contribute to information processing and encoding across brain areas, thereby influencing perception, memory, cognition, and goal-directed behaviours. Notably, impairments in these functions represent some of the earliest hallmarks of ageing and neurodegenerative disorders such as Alzheimer's disease. Here we review molecular, cellular, and computational insights into astrocyte-neuron interactions, framing their importance at the system and behavioural level; then, we discuss the role of these interactions in spatial cognition, goal-directed behaviour, and their impairment in Alzheimer's disease, and review the mouse models used to investigate spatial deficits and associated astrocyte activity. Finally, we highlight major open questions in the field, outline future research directions, and discuss emerging strategies to address astrocyte role in cognitive function in health and disease.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1811370"},"PeriodicalIF":4.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13453706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compassionate-use of autologous, bone marrow-derived mesenchymal stromal cells in a chronic anoxic encephalopathy: a case report.","authors":"Guilherme Lepski, Valeria Modestto, Walker Jeveaux, Daniel Navarro da Rocha, Roberto Dalto Fanganiello, Jose Ricardo Muniz Ferreira, Analia Arevalo","doi":"10.3389/fncel.2026.1822330","DOIUrl":"10.3389/fncel.2026.1822330","url":null,"abstract":"<p><strong>Introduction: </strong>Severe hypoxic-ischemic brain injury may evolve into prolonged disorders of consciousness, for which disease-modifying interventions remain a challenge. Mesenchymal stromal/stem cells (MSCs) are being investigated in neurological disorders predominantly through immunomodulatory and trophic paracrine mechanisms rather than neuronal replacement.</p><p><strong>Methods: </strong>We describe a young adult medicine student with chronic post-anoxic encephalopathy managed under national regulatory oversight for compassionate use of an advanced cellular therapy. Autologous bone marrow-derived MSCs were harvested and expanded under GMP-oriented controls with extensive biosecurity and release testing. Quantitative EEG and source localization with low-resolution electromagnetic tomography (LORETA) were performed before transplantation and 4 months thereafter.</p><p><strong>Results: </strong>Four months after intrathecal administration, subtle but consistent behavioral changes were observed, including more synchronized affective responses, greater environmental engagement, and the first reproducible binary interaction via eye blinking. Retrospective review of available video documentation showed an increase in the Coma Recovery Scale-Revised (CRS-R) score from 8 before treatment to 11 after treatment, with one-point improvements in auditory function, visual function, and arousal. Modified Ashworth Scale spasticity scores improved by 1 in some muscle groups. No adverse events were registered. Longitudinal quantitative EEG demonstrated persistent global slowing compatible with severe diffuse injury, with qualitative emergence of faster activity, high alpha (10-12 Hz) and low beta (12-18 Hz) in bilateral fronto-temporal areas. LORETA current-density maps showed a more anterior distribution of estimated generators toward fronto-limbic regions.</p><p><strong>Discussion: </strong>This case illustrates the feasibility and short-term safety of regulated autologous MSC delivered intrathecally in chronic post-anoxic encephalopathy, while emphasizing that therapeutic efficacy cannot be inferred from a single uncontrolled observation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1822330"},"PeriodicalIF":4.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deletion of the calcium-binding protein S100β alters axon initial segment development in the visual cortex.","authors":"Yanis Inglebert, Rafael Sanz-Gálvez, Danna Quetzali Chavez Lorenzana, Eva Lafaverges, Arlette Kolta","doi":"10.3389/fncel.2026.1895033","DOIUrl":"10.3389/fncel.2026.1895033","url":null,"abstract":"<p><p>The axon initial segment (AIS) is a key structure for fine-tuning neuronal excitability. It plays a particularly important role during development across many sensory systems, where it contributes to network refinement and the adjustment of excitability levels. In the visual cortex, the AIS undergoes a significant period of plasticity that helps adjust neuronal excitability during key developmental stages such as eye opening and the onset of binocular vision. This development is tightly regulated by numerous factors, including glial cells. The calcium-binding protein S100β, which is primarily expressed in astrocytes, has previously been implicated in axonal development. We therefore asked whether it might also contribute to the normal development of the AIS in the visual cortex. Here, we characterize the consequences of S100β loss on AIS development and examine its impact on neuronal excitability.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1895033"},"PeriodicalIF":4.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13453705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A practical CD90.2-based FACS strategy for obtaining Schwann cell-enriched cultures from adult mouse nerves.","authors":"Karen Libberecht, Hanne Jeurissen, Nathalie Dirkx, Yara Lambrechts, Lise Van Horebeek, Koen Kuipers, Femke Reubens, Jana Van Broeckhoven, Tim Vangansewinkel, Esther Wolfs","doi":"10.3389/fncel.2026.1873287","DOIUrl":"10.3389/fncel.2026.1873287","url":null,"abstract":"<p><p>Primary Schwann cell cultures derived from adult murine peripheral nerves are frequently compromised by fibroblast overgrowth, limiting their utility for <i>in vitro</i> studies. Existing enrichment strategies often rely on selective growth conditions, prolonged culture, or antibody-mediated positive selection, which may alter Schwann cell physiology, trigger unwanted signaling, or result in incomplete fibroblast removal. To address these limitations, we developed a reproducible negative selection protocol for the isolation and enrichment of primary adult murine Schwann cells using fluorescence-activated cell sorting (FACS). By specifically targeting contaminating fibroblasts using the marker CD90.2 (Thy-1.2), these cells are efficiently depleted while leaving the Schwann cell population unbound by antibody complexes. This approach enables the rapid generation of highly enriched Schwann cell populations without the need for extended <i>in vitro</i> expansion or antimitotic agents. By avoiding direct receptor-ligand interactions on Schwann cells, this method preserves their native physiological state and surface epitopes, supporting sensitive downstream applications. Successful Schwann cell enrichment was confirmed by quantitative PCR, western blot and immunocytochemistry, demonstrating the enrichment of Schwann cell-specific markers and minimal fibroblast contamination. Overall, this approach enables the rapid generation of highly enriched Schwann cell populations while preserving features relevant to mature Schwann cell biology. This protocol provides a robust and practical tool for researchers requiring physiologically representative adult Schwann cells for molecular, functional, and co-culture-based studies of the peripheral nervous system.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1873287"},"PeriodicalIF":4.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13453763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Technological advances in axonal regeneration and structural plasticity: optogenetics, single-cell omics, and tissue clearing.","authors":"Xiaoqiu Shu, Jiawen Zhang, Zhenwei Qin","doi":"10.3389/fncel.2026.1857896","DOIUrl":"10.3389/fncel.2026.1857896","url":null,"abstract":"<p><p>Modern techniques have provided novel insights into the molecular and structural characteristics of neurons and glial cells in the central nervous system (CNS). Over the past decade, advancements in optogenetics, single-cell RNA sequencing, and tissue clearing have enabled unprecedented resolution, sensitivity, and throughput, driving progress in CNS repair. In this review, we focus on how these technologies have illuminated the dynamic structural and functional behaviors of axons, from degeneration to regeneration, following spinal cord and optic nerve injuries. Optogenetics offers precise spatiotemporal control of neuronal activity, revealing how targeted stimulation influences axonal growth and circuit reorganization. Single-cell omics uncovers the heterogeneity of axonal regenerative capacity among neuronal subtypes and identifies novel regeneration-associated genes (RAGs) that orchestrate axonal structural remodeling. Tissue clearing and 3D imaging allow direct visualization of axonal trajectories, growth cone morphology, and pathfinding errors in intact tissue, overcoming limitations of conventional histology. Together, these approaches have provided important insights into axonal dynamics and have opened new avenues for promoting functional recovery after CNS injury.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1857896"},"PeriodicalIF":4.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut-derived signals regulating glial activation and secondary neuroinflammation after spinal cord injury: an evidence mapping and mechanistic framework.","authors":"Baoxiu Yi, Wenguang Chen, Zhenhai Chi, Qiangjian Mao, Xiaoqin Li, Yuelai Chen","doi":"10.3389/fncel.2026.1897379","DOIUrl":"10.3389/fncel.2026.1897379","url":null,"abstract":"<p><p>Secondary neuroinflammation after spinal cord injury (SCI) is a key pathological process that affects neuronal survival, axonal regeneration, and functional recovery. Increasing evidence suggests that dysbiosis of the gut microbiota, disruption of the intestinal barrier, and abnormal microbial inflammatory and metabolic signals may promote the progression of secondary injury after SCI. However, direct, continuous, and cell-type-specific evidence explaining how gut-derived signals influence glial and neurovascular unit responses within the injured spinal cord through peripheral immune imbalance, blood-spinal cord barrier (BSCB) disruption, and local molecular pathways remains limited. In this narrative review, we organize the existing literature into an evidence map and propose a mechanistic hypothesis: After SCI, autonomic dysfunction, impaired gut motility, and neurogenic bowel dysfunction may disrupt the homeostasis of gut microbiota and barrier, leading to lipopolysaccharide (LPS) overflow, reduced short-chain fatty acids (SCFAs), altered tryptophan metabolism, and increased trimethylamine N-oxide (TMAO). These signals may modulate the responses of microglia/infiltrating macrophages, astrocytes, and the neurovascular unit via peripheral immunity, BSCB, and pathways, including TLR4/NF-κB, NLRP3, and AhR. We also distinguish direct SCI evidence, single-study support, and extrapolated evidence, and specifically avoid presenting the tryptophan metabolite-AhR axis or TMAO-NLRP3 axis as established SCI pathways. Overall, the gut-spinal cord axis may provide a useful framework for understanding and targeting secondary neuroinflammation after SCI. Still, its causal chain, temporal characteristics, and cell-specific effects require further validation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1897379"},"PeriodicalIF":4.4,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13447481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148688747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}