Frontiers in Cellular Neuroscience最新文献

{"title":"Correction: Histone deacetylase inhibitors are protective in acute but not in chronic models of ototoxicity.","authors":"Chao-Hui Yang, Zhiqi Liu, Deanna Dong, Jochen Schacht, Dev Arya, Su-Hua Sha","doi":"10.3389/fncel.2026.1819319","DOIUrl":"https://doi.org/10.3389/fncel.2026.1819319","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2017.00315.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1819319"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13081227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697970","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":"\"Mind the Gap\"-enlarged perivascular spaces as a potential magnetic resonance imaging biomarker of impaired glymphatic clearance in brain disorders.","authors":"Claudia F Kirsch, Mackenzie Herb, Guarav Verma, Priti Balchandani","doi":"10.3389/fncel.2026.1741115","DOIUrl":"https://doi.org/10.3389/fncel.2026.1741115","url":null,"abstract":"<p><p>The abundant capillary network penetrating the brain parenchyma is surrounded by potential tubular, fluid-filled regions referred to as perivascular spaces (PVSs). PVSs have a unique and complex history and are believed to act as a pathway for the drainage of waste products from brain interstitial and cerebrospinal fluid (CSF) as part of the glymphatic clearance system. The unique perivascular \"gap\" spaces are eponymously linked to Virchow and Robin, who argued vigorously in the 1800s over PVSs' exact location and physiology. Currently, debates are ongoing regarding whether PVSs are predominantly periarteriolar, perivenular, or both and how they aid in clearing fluids from the brain parenchyma. In neurodevelopmental, neuropsychiatric, and neuropathological conditions, PVS can enlarge, a phenomenon referred to as enlarged perivascular spaces (ePVSs), which are identifiable on magnetic resonance imaging (MRI), with improved detection and resolution at higher magnetic field strengths. Quantification of ePVS enlargement on MRI using artificial intelligence (AI) imaging algorithms may serve as a potential non-invasive imaging biomarker for impaired glymphatic clearance and brain disorders. This mini-review presents the historical background and pathophysiology of PVSs and ePVSs, current debates regarding their exact location, their potential as neuroimaging biomarkers, and how AI may aid in ePVS quantification.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1741115"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13079593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698036","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":"Contribution of proprioceptors in the mesencephalic trigeminal nucleus and their surrounding astrocytes to acidic saline-induced chronic jaw muscle pain in rodents.","authors":"Masaharu Yamada, Dorly Verdier, Arlette Kolta","doi":"10.3389/fncel.2026.1800565","DOIUrl":"https://doi.org/10.3389/fncel.2026.1800565","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic jaw muscle pain is a common clinical condition whose etiology remains ill-defined. Using acidic saline injections into the masseter muscle to mimic it, we examined the hypothesis that hyperexcitability of jaw closing muscles spindle afferents (MSA) that have previously been observed in this model result from neuron glia interactions in the trigeminal mesencephalic nucleus (NVmes) lead to activation of nociceptive pathways.</p><p><strong>Methods: </strong>This was assessed using whole-cell patch-clamp recordings from NVmes neurons combined to pharmacological and astrocytic optogenetic stimulations and immunohistochemistry against cFos in the ventrolateral pole of the subnucleus interpolaris/caudalis transition region (vl-Vi/Vc), and GFAP in vl-Vi/Vc and NVmes regions in rats and mice.</p><p><strong>Results: </strong>Acidic saline injection into the masseter muscle led to increases in: (1) cFos expression in vl-Vi/Vc at 9 days after the injection, (2) reactivity of astrocytes in NVmes, and (3) Excitability of NVmes neurons that manifested spontaneously or in response to astrocytic stimulation. This increased activity is thought to result from the release of the astrocytic Ca²⁺-binding protein S100β, since it was not observed in S100β knock-out mice, which also did not show increased expression of cFos in vl-Vi/Vc, despite showing increased reactivity of NVmes astrocytes.</p><p><strong>Discussion: </strong>These findings suggest that acidic saline injection into the masseter muscles induced long-term activation of astrocytes in the NVmes and promoted ectopic firing of NVmes neurons via astrocyte-released S100β, and subsequent activation of nociceptive pathways.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1800565"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13079590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697977","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":"Systematic review of literature regarding the isolation of mesenchymal adult stem cells from the olfactory epithelium.","authors":"Carlotta Pipolo, Paula La Rubia, Anna Cozzi, Preetha Karki, Alberto Maria Saibene, Daniele Bottai","doi":"10.3389/fncel.2026.1735284","DOIUrl":"https://doi.org/10.3389/fncel.2026.1735284","url":null,"abstract":"<p><strong>Background: </strong>The olfactory mucosa has emerged as a promising source of mesenchymal stem cells with neurogenic potential. These cells exhibit neural, glial, and mesenchymal properties, making them attractive candidates for regenerative medicine, particularly in treating neurodegenerative and immunemediated disorders.</p><p><strong>Methods: </strong>This systematic review analyzed existing literature on the isolation, characterization, and therapeutic applications of olfactory mucosa mesenchymal stem cells. The review assessed variations in isolation techniques, culture conditions, and differentiation potential, as well as preclinical and clinical applications.</p><p><strong>Results: </strong>Olfactory mucosa mesenchymal stem cells express key neural and mesenchymal markers, including Nestin, SRY-box 2, <i>Glial Fibrillary Acidic protein</i>, CD44, and CD105, confirming their multilineage differentiation capacity. Their ability to secrete neurotrophic factors such as Brain-Derived Neurotrophic Factor, Nerve Growth Factor, and Glial Cell Derived Neurotrophic Factor underscores their role in neural repair. While most studies successfully isolated olfactory mucosa mesenchymal stem cells via biopsy, differences in sampling depth and culture media influenced cell yield and growth patterns. Preclinical studies suggest that olfactory mucosa mesenchymal stem cells (OM-MSCs) may represent a promising experimental model for neurological disorders-including Parkinson's disease, spinal cord injury, schizophrenia, and retinal diseases-although current evidence remains preliminary and translational efficacy has not yet been established. However, challenges remain in standardizing protocols, addressing donor variability, and ensuring clinical safety.</p><p><strong>Conclusion: </strong>Olfactory mucosa mesenchymal stem cells represent a promising avenue for neurological and regenerative therapies. Despite their potential, further research is needed to optimize isolation techniques, enhance reproducibility, and navigate regulatory hurdles. Collaborative efforts between researchers, clinicians, and regulatory bodies will be essential to translating OM-MSC research into viable clinical applications.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1735284"},"PeriodicalIF":4.0,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688552","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 neurobiological regulatory mechanism of brain edema.","authors":"Meiqi Tian, Man Li, Chaoying Zhang, Qi Luo, Aiwen Wang, Dongyang Li","doi":"10.3389/fncel.2026.1777039","DOIUrl":"https://doi.org/10.3389/fncel.2026.1777039","url":null,"abstract":"<p><p>Cerebral edema is a common pathological condition associated with a variety of neurological disorders, and its development involves numerous neurobiological mechanisms. This review explores the neurobiological regulatory mechanisms underlying cerebral edema, including the disruption of the blood-brain barrier, inflammatory responses, alterations in vascular permeability, and intracellular edema. We will investigate the formation mechanisms of cerebral edema under different pathological states and discuss potential therapeutic strategies, aiming to provide insights for clinical treatment. Current research highlights the complexity of the interactions between these mechanisms and the need for targeted interventions to mitigate the impact of cerebral edema on patient outcomes. This review aims to synthesize existing knowledge and encourage further exploration in this critical area of neuroscience, ultimately contributing to more effective management of cerebral edema.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1777039"},"PeriodicalIF":4.0,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688588","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":"Editorial: Reviews in non-neuronal cells 2024 & 2025.","authors":"Qingchao Qiu, Bo Hu","doi":"10.3389/fncel.2026.1825487","DOIUrl":"10.3389/fncel.2026.1825487","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1825487"},"PeriodicalIF":4.0,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671883","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":"Immaturity of the neuromuscular junction in spinal muscular atrophy mouse models.","authors":"Lucía Tabares, Andrea Fuentes-Moliz, Raquel Cano, Rocío Ruiz, Saravanan Arumugam","doi":"10.3389/fncel.2026.1795130","DOIUrl":"https://doi.org/10.3389/fncel.2026.1795130","url":null,"abstract":"<p><p>Spinal muscular atrophy (SMA) is caused by deficiency of the survival motor neuron (SMN) protein and is classically defined by degeneration of lower motor neurons. Extensive evidence from mouse models and human tissue demonstrates that dysfunction at the neuromuscular junction (NMJ) emerges early and precedes overt denervation. Here, we review structural, molecular, and functional studies showing that SMA NMJs fail to complete key postnatal maturation programmes that normally scale presynaptic release capacity to muscle growth and increasing functional demand. SMA motor terminals retain multiple features of developmental immaturity, including reduced active zone number, limited synaptic vesicle pool extension, altered cytoskeletal organisation, incomplete molecular specialization, and impaired recruitment of functional release sites, resulting in constrained neurotransmitter release and reduced presynaptic reserve. These defects are highly muscle- and region-specific and preferentially affect vulnerable motor units. We propose a conceptual framework in which delayed and incomplete NMJ maturation increases susceptibility to superimposed degenerative processes, ultimately leading to synaptic destabilisation and denervation. This integrated view reconciles early synaptic dysfunction with later neurodegeneration and has important implications for understanding SMA pathogenesis, identifying sensitive biomarkers, and optimizing the timing and targets of therapeutic intervention.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1795130"},"PeriodicalIF":4.0,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671863","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 GPR68-NINJ1 axis: an emerging mechano-chemical checkpoint in blood-brain barrier disruption-a hypothetical framework and therapeutic promise.","authors":"Boren Bai, Haixiao Feng, Huimin Yang, Maokui Huang, Yuechun Wang","doi":"10.3389/fncel.2026.1757822","DOIUrl":"https://doi.org/10.3389/fncel.2026.1757822","url":null,"abstract":"<p><p>The blood-brain barrier (BBB) is a critical interface whose failure is a convergent pathological feature of traumatic, ischemic, and neurodegenerative neurological diseases. Current paradigms often overlook the synergistic interplay between mechanical forces and biochemical cues, such as acidosis, that drive BBB disruption. This perspective synthesizes groundbreaking, yet largely independent, discoveries on two key molecules: GPR68 (OGR1), a proton-sensing GPCR with unique millisecond-level mechanosensitivity to shear stress, and NINJ1, a recently defined executor of plasma membrane rupture during lytic cell death. We propose a testable novel hypothesis: that these proteins form a functional \"GPR68-NINJ1 axis,\" creating a self-amplifying mechano-chemical circuit that initiates and exacerbates BBB breakdown. We detail the molecular logic of this axis-from GPR68's sensing of pathological acidosis (pH ≤ 6.4) and shear stress to NINJ1's oligomerization and DAMP release-and explore its potential role in unifying the pathophysiology of diverse disorders like TBI, stroke, MS, and AD. Finally, we translate this framework into a roadmap for future research and therapeutic intervention, discussing targeted inhibitors, precision chronotherapy, and the critical experiments needed to validate this emerging paradigm.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1757822"},"PeriodicalIF":4.0,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670591","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":"Recreating the human brain: Are assembloids merely descriptive models?","authors":"Yara Izhiman, Charitha Anamala, Eric A Nauman, Volha Liaudanskaya","doi":"10.3389/fncel.2026.1787173","DOIUrl":"https://doi.org/10.3389/fncel.2026.1787173","url":null,"abstract":"<p><p>Assembloids, engineered fusions of region-specific brain 3D constructs, have emerged as powerful platforms to study neurodevelopment and neurological diseases. Unlike first-generation organoids, assembloids enable direct modeling of interregional communication, allowing investigation of higher-order brain functions that depend on circuit-level interactions. Over the past 5 years, rapid advances in human-derived assembloid systems have demonstrated their ability to recapitulate key features of human brain organization, including long-range projection formation, region-specific signaling, neurovascular coupling, and progressive network dysfunction. The primary application of assembloid modeling remains the study of neurodevelopment, specifically focusing on mapping biological mechanisms driving the human brain development. Another major application of assembloids is the study and modeling of neurological diseases. Recent studies have integrated multiple neural regions, alongside vascular and glial components, and disease-relevant genetic backgrounds to recreate circuit-level interactions underlying pathology. These approaches have further highlighted the importance of neuroglial interactions in shaping development, connectivity, and disease progression in the human brain. Across models and disease contexts, a consistent theme has emerged: pathological phenotypes arise primarily from disrupted intercellular communication rather than isolated cellular and more purely neuronal, defects. Despite these strengths, current assembloid platforms remain limited by incomplete maturation, variability in reproducibility, and challenges in modeling long-term disease trajectories. Together, existing evidence positions assembloids as a promising next-generation platform for studying human brain development and neurodegeneration, while highlighting the need for continued refinement to improve physiological relevance as model complexity increases.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1787173"},"PeriodicalIF":4.0,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13065703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670638","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":"Neuropeptide and cytokines expression in long COVID-19 related neuropsychological sequelae: insights into NK1R-mediated neuroinflammation and <i>in silico</i> therapeutic targeting.","authors":"Muhammad Abdullah, Anam Naz, Leah R Reznikov, Javed Anver Qureshi, Ammarah Hasnain, Ayesha Obaid, Amjed Ali","doi":"10.3389/fncel.2026.1763029","DOIUrl":"https://doi.org/10.3389/fncel.2026.1763029","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Long COVID-19 causes neurophysiological, cardiopulmonary, and musculoskeletal issues. Increased neuropeptides and cytokines lead to neuroinflammation, resulting in neurocognitive impairments, fatigue, depression, anxiety, and severe cognitive deficits. The Neurokinin 1 receptor (NK1R) is a cellular receptor for the neuropeptide Substance P, and its dysregulation links to neuropsychological issues despite antipsychotic use.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;In the present study, neuropsychological sequelae related to long COVID-19 were screened and the expression of related neuropeptides and cytokines was evaluated. Additionally, potential drugs have been evaluated computationally to reduce neuroinflammation in long COVID-19.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;After informed consent, subjects were screened by a medical physician for long COVID-19 in an outdoor patient clinic. Various biological scales were used to assess and categorize the severity of neuropsychological symptoms related to long COVID-19. After that, peripheral blood samples were collected from subjects using ELISA and RT-qPCR. Nine drugs were selected and subjected to virtual screening to identify potential drug antagonists for NK1R. The key drug-like properties, safety profile, pharmacokinetic analysis, and biological activity of the identified hits were assessed.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In this study the mean age of 90 patients (60% males and 40% females), was 33 ± 5 years in the symptomatic group and 31 ± 6 years in the asymptomatic long COVID-19 group for &lt;40 years age-group. Whereas, the mean age of &gt;40 years age-group was 58 ± 10 years in the symptomatic group and 54 ± 11 years in the asymptomatic long COVID-19 group. The minimum persistence of duration of long COVID-19 related symptoms in the &lt;30 weeks group was observed to be 19 ± 6 weeks, while 44 ± 6 weeks in the &gt;30 weeks group of symptomatic long COVID-19. A total of 48% patients had fatigue, 47% complained about headache, 28% had anxiety, 25% faced depression, 20% had psychosocial distress, 20% felt discomfort, and 13% had cognitive impairment. A total of 10% had reported dizziness sequelae among long COVID-19 survivors. Experimental data showed upregulation of IL-6, IL-10, and SP in both symptomatic and asymptomatic individuals compared with controls (&lt;i&gt;p&lt;/i&gt; &lt; 0.001). Drug screening analyses revealed aprepitant (-9.3 kcal/mol) and N- acetyl- L- tryptophan (-8.7 kcal/mol) stable interactions with NK1R and maintaining molecular dynamics stability (RMSD: 1.5-2.2 Å; RMSF 0.8-1.4 Å; Rg approximately 21.6 Å). These compounds also demonstrated favorable blood-brain barrier permeability and pharmacokinetic profiles, suggesting their potential as therapeutic antagonists for treating prolonged COVID-related neuroinflammation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;IL-6, IL-10, and SP are found to be deregulated in long COVID-19 leading to neurophysiological sequelae. To overcome neuropsychol","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1763029"},"PeriodicalIF":4.0,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13061724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671881","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}