Frontiers in Cellular Neuroscience最新文献

{"title":"The grand challenge in cellular neurophysiology.","authors":"Björn Kampa, Arianna Maffei","doi":"10.3389/fncel.2026.1980835","DOIUrl":"10.3389/fncel.2026.1980835","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1980835"},"PeriodicalIF":4.4,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135552","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":"Efficacy of anticoagulation therapy in elderly patients with clinically diagnosed Alzheimer's disease and atrial fibrillation: a clinical outcomes study.","authors":"Xinhui Wang, Xinying Yang, Yiman Huang, Peng Qian, Hongyan Duan","doi":"10.3389/fncel.2026.1874032","DOIUrl":"10.3389/fncel.2026.1874032","url":null,"abstract":"<p><strong>Introduction: </strong>Clinically diagnosed Alzheimer's disease (AD) and atrial fibrillation (AF) are prevalent in the elderly, and their co-occurrence presents a complex management dilemma, balancing stroke prevention against bleeding risks, particularly in the context of cognitive impairment. This real-world cohort study aimed to evaluate the clinical outcomes of anticoagulant therapy in elderly patients with AD and AF.</p><p><strong>Methods: </strong>We analyzed data from 342 patients (mean age 78.5 years; 58.3% female) with non-valvular AF and AD. Patients were categorized into anticoagulant (<i>n</i> = 247; 72.2%) and non-anticoagulant (<i>n</i> = 95; 27.8%) groups, with direct oral anticoagulants (DOACs) used in 57.9% of treated patients. Over a mean follow-up of 2.1 years, outcomes were compared between groups.</p><p><strong>Results: </strong>Anticoagulation was associated with a significantly lower incidence of ischemic stroke/systemic embolism (annualized rate 2.9% vs. 7.1%; hazard ratio [HR] = 0.35, 95% CI 0.17-0.73, <i>p</i> = 0.005) and all-cause mortality (6.3% vs. 15.1%; HR = 0.32, 95% CI 0.19-0.54, <i>p</i> < 0.001) compared to no anticoagulation. DOACs were superior to warfarin in preventing stroke/embolism (HR = 0.36, 95% CI 0.15-0.87, <i>p</i> = 0.022). While major bleeding was higher with anticoagulation (6.1% vs. 0.9%; HR = 4.31, 95% CI 1.02-18.19, <i>p</i> = 0.047), the critical risk of intracranial hemorrhage was not significantly increased (1.6% vs. 1.0%; HR = 0.46, 95% CI 0.11-1.98, <i>p</i> = 0.30), and DOACs demonstrated a safer profile versus warfarin for major bleeding (HR = 0.24, 95% CI 0.06-0.89, <i>p</i> = 0.034). Key predictors for bleeding and thromboembolism, for example, advanced age, previous stroke history, and high HAS-BLED scores, were identified.</p><p><strong>Discussion: </strong>In conclusion, anticoagulation, particularly with DOACs, provides a favorable net clinical benefit by significantly reducing stroke and mortality without a marked increase in intracranial hemorrhage in elderly AD patients with AF, supporting its judicious use. Further prospective studies are warranted to refine personalized decision-making.</p><p><strong>Systematic review registration: </strong>https://www.crd.york.ac.uk/PROSPERO/view/CRD420251271276, Identifier: CRD420251271276.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1874032"},"PeriodicalIF":4.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127079","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":"Primary cilia as a molecular convergence hub linking neurodevelopment and autism spectrum disorder.","authors":"Arianna Boscato, Lorenzo Milesi, Marta Biagioli, Alice Tata","doi":"10.3389/fncel.2026.1914796","DOIUrl":"10.3389/fncel.2026.1914796","url":null,"abstract":"<p><p>The primary cilium, a highly conserved microtubule-based organelle, orchestrates a broad repertoire of signal transduction cascades required for embryonic development, tissue homeostasis and cellular communication. Disruption of ciliary structure or function results in a heterogeneous group of multisystem disorders known as ciliopathies. Emerging genomic and transcriptomic evidence indicates that perturbation of ciliary architecture or signaling may also contribute to neurodevelopmental conditions and specifically to autism spectrum disorder (ASD). Genes linked to ASD show a wide range of genetic and phenotypic characteristics: spanning from syndromic neurodevelopmental disorders with overlapping ciliopathy features to idiopathic ASD. Yet the mechanistic contribution of ASD risk genes to ciliary biology remains insufficiently characterized. This study aims to explore the molecular convergence between ciliopathies and ASD by systematically interrogating ciliary gene datasets (CiliaCarta and SysCilia GSv2) in cross-comparison to ASD-associated gene repositories (SFARI Gene). This integrative analysis identifies 105 high-confidence shared genes, which segregate into four mechanistic modules: (i) structural determinants of cilium assembly and maintenance, (ii) components of cilium-dependent signaling pathways, (iii) regulators of cilium-associated gene expression and (iv) cilium associated pathways. We propose that ciliary dysfunction constitutes a convergent mechanism, perturbing neurodevelopmental signaling, neuronal polarity and synaptic maturation in a subset of ASD cases. Clarifying the role of the genes shared between ciliogenesis and neurodevelopmental signaling will refine genotype-to-phenotype correlations, expand the spectrum of cilia-associated neurodevelopmental disorders and potentially uncover therapeutically actionable hubs within cilium-dependent signaling circuitry.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1914796"},"PeriodicalIF":4.4,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135589","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":"Research hotspots and emerging trends of macrophages in peripheral nerve injury: a bibliometric and visualization analysis.","authors":"Guohua Jiang, Renkun Huang, Kewen Wang, Yuchang Gui, Yun Tang, Guiyang Jiang, Yijun Liu, Jianwen Xu","doi":"10.3389/fncel.2026.1893849","DOIUrl":"https://doi.org/10.3389/fncel.2026.1893849","url":null,"abstract":"<p><strong>Objective: </strong>Peripheral nerve injury (PNI) remains a significant clinical challenge due to its poor neurological recovery. Macrophages serve as key regulators in pathological degeneration, inflammatory resolution, and regenerative repair after PNI. This study aims to explore the global status, research hotspots, and developmental trends of macrophage-related studies in PNI through bibliometric analysis. It further aimed to identify emerging research frontiers and existing knowledge gaps, thereby providing insights into optimized PNI repair strategies.</p><p><strong>Methods: </strong>Literature related to PNI and macrophages published from January 1, 2006, to March 31, 2026, was retrieved from the Web of Science Core Collection and Scopus databases. After literature screening, deduplication, and data standardization, VOSviewer, CiteSpace, and Bibliometrix were used to perform bibliometric analysis and visualization of countries, institutions, authors, journals, keywords, and citations.</p><p><strong>Results: </strong>A total of 694 publications were included. The annual publication output showed a continuous upward trend, with a marked increase after 2017 and a peak of 76 publications in 2025. A total of 50 countries contributed to this field. China had the highest number of publications, whereas the United States had the highest total number of citations. Nantong University was the most productive institution, and Kiguchi, Norikazu and Kishioka, Shiroh were the most productive authors. <i>Journal of Neuroinflammation</i> was the leading journal in this field. Macrophage polarization, Wallerian degeneration, neuropathic pain, macrophage-Schwann cell interactions, immunomodulation, and inflammatory microenvironment remodeling were the long-standing core hotspots in this field. In recent years, subcellular injury and neural excitability mechanisms, including apoptosis and efferocytosis, mitochondrial dysfunction, and ion channels, have received increasing attention. Tissue engineering and biotherapeutic strategies, such as nerve conduits, mesenchymal stem cells, exosomes, and drug delivery, have become emerging research directions. Moreover, the application of transcriptomics and single-cell RNA sequencing has further advanced the in-depth analysis of macrophage heterogeneity and molecular regulatory mechanisms.</p><p><strong>Conclusion: </strong>This study revealed the hotspots and trends of macrophage research in PNI over the past two decades. Research foci have expanded from basic pathological mechanisms to neuroimmune regulation and regenerative strategies. Combined omics and bioinformatics will help elucidate macrophage regulatory networks and advance precise interventions for PNI.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1893849"},"PeriodicalIF":4.4,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106530","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":"Brain endothelial homeostasis in psychiatric disorders: mechanisms, evidence, and translational opportunities.","authors":"Mengjie Zhang, Xueying Huang, Lin Yao, Wenqing Wu","doi":"10.3389/fncel.2026.1901256","DOIUrl":"https://doi.org/10.3389/fncel.2026.1901256","url":null,"abstract":"<p><p>Brain endothelial cells (BECs) are specialized components of the neurovascular unit that couple circulating signals to cerebral blood flow regulation, blood-brain barrier (BBB) function, and selective molecular transport. This narrative review evaluates the correlation of these endothelial functions with psychiatric disorders, including depression and schizophrenia, distinguishing established vascular physiology from disease-specific evidence. In neurovascular coupling, the functions of capillary Kir2.1/phosphatidylinositol 4,5-bisphosphate and ATP-sensitive K⁺ channels, TRPA1-PANX1-P2X signaling, inositol 1,4,5-trisphosphate receptor-mediated Ca²⁺ events, arterial GJA4/GJA5 coupling, and PIEZO1-mediated mechanical feedback vary depending on the vascular segment. At the BBB, CLDN5, OCLN, F11R, TJP1, CDH5, the actin cytoskeleton, MFSD2A, and selective influx and efflux transporters determine paracellular permeability and transcytosis. Cerebral fluid and solute clearance should be separated into perivascular cerebrospinal fluid/interstitial fluid exchange, BBB transport, and meningeal lymphatic or venous drainage. BECs contribute to vascular and transporter interfaces but are not demonstrated to be the central drivers of glymphatic flow. Stress-related, sex-dependent, and brain region-dependent changes in CLDN5 and endothelial inflammatory signaling are reported to be strongly correlated with psychiatric disorders. In contrast, studies on serum biomarkers, postmortem tissues, patient-derived models, and animals provide different and non-equivalent levels of inference. Clinical trials have not evaluated a BEC-directed therapy for a primary psychiatric disorder. Future studies must focus on developing endothelial-specific and vascular segment-specific interventions, identifying prospective human BBB or cerebrovascular biomarkers, performing analysis according to sex and brain region, and systematically assessing peripheral vascular and barrier-related safety.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1901256"},"PeriodicalIF":4.4,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106021","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":"Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.","authors":"Mingrui Song, Nan Bu, Long Wei, Jing Chen","doi":"10.3389/fncel.2026.1945478","DOIUrl":"10.3389/fncel.2026.1945478","url":null,"abstract":"<p><p>Post-ischaemic white-matter injury involves axonal dysfunction, myelin disorganization, delayed accumulation of myelin-derived debris, and an often incomplete regenerative response. Microglia provide a cellular link between debris clearance and white-matter repair through a sequence of functionally distinct processes encompassing selective debris recognition, internalization, intracellular degradation, lipid handling, inflammatory regulation, and oligodendroglial support. Importantly, increased myelin uptake should not be equated with successful clearance, and clearance itself does not establish effective remyelination. This review prioritizes direct evidence from adult ischaemic stroke while using studies from related white-matter and demyelination models to clarify defined cellular or metabolic steps as mechanistic context rather than as stroke-equivalent evidence. Available evidence indicates that OPC recruitment and early lineage responses are frequently preserved after stroke, whereas terminal oligodendrocyte maturation and structurally competent myelin reconstruction remain limiting steps. Within microglia, lysosomal competence and post-phagocytic lipid processing emerge as critical intermediate bottlenecks that determine whether internalized myelin is successfully disposed of or instead promotes lipid accumulation, inflammatory dysfunction, and impaired oligodendroglial support. Direct adult-stroke evidence nevertheless remains substantially more limited than the broader mechanistic literature derived from related experimental systems. We therefore propose that repair-relevant microglial activity should be evaluated across sequential checkpoints-from selective recognition and intracellular processing to lipid disposal, oligodendroglial maturation, and structurally and functionally validated remyelination.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1945478"},"PeriodicalIF":4.4,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080239","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":"Exploring epigenetic modifications following maternal immune activation: a focus on cross-species translational potential.","authors":"Felisa J Carbajal, Janine M LaSalle, Melissa D Bauman","doi":"10.3389/fncel.2026.1941243","DOIUrl":"10.3389/fncel.2026.1941243","url":null,"abstract":"<p><p>Maternal infection during pregnancy has emerged from epidemiological research as a key factor in the risk for neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD) and schizophrenia (SZ). Animal models provide translational tools to explore mechanisms linking maternal infection with altered offspring neurodevelopment. Maternal immune activation (MIA) models have been used to systematically explore the associations between specific maternal cytokines, <i>in vivo</i> measures of offspring brain, behavior and immune system development, and ultimately, to identify cellular and molecular changes that underly aberrant offspring neurodevelopment. Emerging evidence from rodent MIA models suggests that prenatal immune challenge induces NDD-relevant phenotypes not only in directly exposed individuals but also their descendants, suggesting that the public health consequences of MIA may be exponentially greater than previously understood. Epigenetic mechanisms have emerged as a critical, but understudied, area of research in the MIA field. Although epigenomic mechanisms could explain long-lived lifetime and intergenerational effects associated with maternal infection, there are limitations in translating epigenetic findings from preclinical rodent MIA models to humans. Here, we summarize the preclinical rodent studies investigating the effects of MIA on the offspring epigenome and highlight the translational potential of emerging data from non-rodent MIA models.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1941243"},"PeriodicalIF":4.4,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080252","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":"Stress-induced tunneling nanotube communication in CNS glial cells: implications for inflammatory demyelination and repair failure.","authors":"Yanjun Liu, Mingming Li, Wei Liu, Jia Guo, Jian Yin","doi":"10.3389/fncel.2026.1949981","DOIUrl":"10.3389/fncel.2026.1949981","url":null,"abstract":"<p><p>Multiple sclerosis and related inflammatory demyelinating disorders of the central nervous system, including neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease, are characterized by immune-mediated tissue injury, glial dysfunction, metabolic stress, and incomplete repair. Although peripheral immune infiltration and antibody-mediated mechanisms explain many aspects of acute lesion formation, they do not fully account for persistent lesion activity, metabolic instability, or remyelination failure within the local tissue microenvironment. Tunneling nanotubes are thin, actin-rich membranous connections that enable direct intercellular transfer of organelles, vesicles, proteins, ions, and stress-related cargoes. In the nervous system, tunneling nanotube-mediated communication has been implicated in mitochondrial transfer, glial-neuronal interactions, pathological cargo dissemination, and cellular stress adaptation. This review examines the potential role of tunneling nanotubes in multiple sclerosis and related inflammatory demyelinating disorders from a lesion-centered perspective. Moving beyond general descriptions of TNT biology, glial communication, and mitochondrial transfer, we consider how TNT-mediated intercellular exchange may intersect with pathological cargo transfer, metabolic stress and support, neurovascular dysfunction, and impaired repair within demyelinating lesions. In multiple sclerosis, they may be particularly relevant to chronic active lesion edges, glial stress responses, and remyelination failure. In aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder, they may be more closely related to astrocytic injury and neurovascular-unit stress. In myelin oligodendrocyte glycoprotein antibody-associated disease, their potential relevance is more speculative and may lie in post-inflammatory repair coordination. Direct evidence remains limited. Future studies should prioritize rigorous <i>in situ</i> identification, cell-type-specific analysis, cargo tracking, and causal intervention experiments before tunneling nanotubes can be considered a validated disease mechanism.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1949981"},"PeriodicalIF":4.4,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080323","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":"Correction: Reward contingency reorganizes lateral orbitofrontal cortex pyramidal neuron activity from reward-aligned to action-aligned during associative learning.","authors":"Zicheng Yang, Xiaolan Chen, Xiaohong Sun, Huimeng Lei","doi":"10.3389/fncel.2026.1987114","DOIUrl":"https://doi.org/10.3389/fncel.2026.1987114","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2026.1850197.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1987114"},"PeriodicalIF":4.4,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149059614","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":"Deciphering the impact of genetic variants on vulnerability to Opioid Use Disorder.","authors":"Rajashree Chakraborty, Chittibabu Guda, Avinash Veerappa","doi":"10.3389/fncel.2026.1814602","DOIUrl":"10.3389/fncel.2026.1814602","url":null,"abstract":"<p><strong>Introduction: </strong>Opioid Use Disorder (OUD) is a chronic condition characterized by compulsive opioid intake that drives widespread health, social, and economic burdens.</p><p><strong>Methods: </strong>To elucidate molecular contributors to addiction susceptibility, we conducted a comprehensive RNA-sequencing analysis of postmortem nucleus accumbens (NAc) tissue from individuals with OUD and matched controls.</p><p><strong>Results: </strong>Cohort-concordance filtering identified 17 candidate missense variants and one candidate stop-gain variant across 16 genes detected in OUD samples; these RDEVs require DNA-based validation. Missense variants could disrupt key protein domains, and five of these identified variants (<i>FUT9, FMR1, MFN1, RYR3</i>, and <i>DAG1</i>) have been previously linked to Substance Use Disorders (SUDs) traits. The only stop-gain variant, <i>ZNF117</i>, was predicted to produce a truncated protein via impaired folding. Transcriptomic profiling followed by Ingenuity Pathway Analysis (IPA) predicted activation of neurodevelopmental programs, with 145 upregulated and 29 downregulated genes collectively implicating pathways related to synaptic plasticity, neuronal differentiation, and axon guidance. Importantly, differential expression of long non-coding RNAs (lncRNAs), including <i>LINC01554</i> and <i>LINC00996</i>, was identified, with putative regulatory associations with key transcription factors (TFs) such as <i>NPAS4</i> and <i>GADD45B</i>.</p><p><strong>Discussion: </strong>Together, these findings provide an integrated view of candidate genetic and transcriptomic alterations in OUD and identify lncRNA-centered regulatory networks and candidate variant-bearing genes as hypothesis-generating leads for future functional and DNA-based validation studies.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1814602"},"PeriodicalIF":4.4,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13600877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149037162","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}