Molecular Neurobiology最新文献

{"title":"Astrocyte-Derived Extracellular Vesicles and the Evolution of Neural Complexity: Perspectives on Vesicle-Mediated Neuron-Glia Communication.","authors":"Katarzyna Ciuba","doi":"10.1007/s12035-026-06214-y","DOIUrl":"10.1007/s12035-026-06214-y","url":null,"abstract":"<p><p>The classic view of neural communication occurring exclusively via synapses has been challenged by growing evidence that glial cells, in particular astrocytes, play an active role in shaping neural circuits. Astrocytes impact neural networks via distinct mechanisms, some of them remaining elusive. Here, we discuss the role of astrocyte-derived extracellular vesicles (ADEVs) and their possible functions in complementing intercellular communication in parallel with synaptic communication and direct gliotransmission. Because astrocytes have undergone substantial evolutionary expansion and diversification in mammals, we also draw the perspective that frames ADEVs within an evolutionary context. We posit that ADEV-mediated signaling may represent an additional candidate axis of astrocyte-neuron communication and discuss testable predictions this hypothesis generates.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081613","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":"Correction to: Caveolin-1 Ablation Imparts Partial Protection Against Inner Retinal Injury in Experimental Glaucoma and Reduces Apoptotic Activation.","authors":"Mojdeh Abbasi, Vivek K Gupta, Nitin Chitranshi, Veer B Gupta, Mehdi Mirzaei, Yogita Dheer, Linda Garthwaite, Thiri Zaw, Robert G Parton, Yuyi You, Stuart L Graham","doi":"10.1007/s12035-026-06235-7","DOIUrl":"https://doi.org/10.1007/s12035-026-06235-7","url":null,"abstract":"","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREM2 Attenuates Microglial Pyroptosis in Sepsis-Associated Encephalopathy Through Modulation of the mtDNA-cGAS-STING Pathway.","authors":"Peng Wang, Hanhong Zhuang, Jiemei Li, Xuemei Song, Siyi Wu, Yuanjie He, Jing He, Xian Qiu, Fei Lin","doi":"10.1007/s12035-026-06230-y","DOIUrl":"10.1007/s12035-026-06230-y","url":null,"abstract":"<p><p>Microglial pyroptosis and the ensuing neuroinflammation are increasingly recognized as important contributors to sepsis-associated encephalopathy (SAE). Triggering receptor expressed on myeloid cells 2 (TREM2) has been implicated in sepsis-related neuroinflammation and SAE; however, how TREM2 is linked to microglial pyroptosis remains incompletely understood. This study aimed to investigate the potential involvement of the mtDNA-cGAS-STING pathway in TREM2-associated regulation of microglial pyroptosis in SAE. An SAE mouse model was established by intraperitoneal injection of lipopolysaccharide (LPS), and an in vitro microglial pyroptosis model was generated in BV2 cells using LPS/nigericin. TREM2 knockout led to more severe neuronal damage and cognitive impairment in LPS-challenged mice. In vivo, TREM2 deficiency was associated with enhanced hippocampal microglial pyroptosis and inflammatory cytokine release, and TREM2 knockdown promoted pyroptosis and inflammatory responses in BV2 microglial cells in vitro. Mechanistically, our in vitro data suggest that TREM2 helps maintain mitochondrial homeostasis, reduces the accumulation of mitochondrial DNA (mtDNA) in the cytosol, and suppresses activation of the cGAS-STING pathway. Depletion of mtDNA with ethidium bromide (EtBr) partially reversed TREM2 knockdown-induced cGAS-STING overactivation, reduced pyroptosis and inflammatory cytokine release, and alleviated microglia-associated neuronal injury. Together, these findings suggest that TREM2 is associated with reduced microglial pyroptosis and microglia-associated neuronal injury in SAE, and that mtDNA-cGAS-STING signaling may participate in this process.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive-Motor Dual Task Training Synergistically Improves Aging-related Cognitive Dysfunction By Reducing TMAO and Suppressing TXNIP/NLRP3 Pathway.","authors":"Rong Zhang, Tengteng Dai, Ziman Zhu, Weijun Gong","doi":"10.1007/s12035-026-06228-6","DOIUrl":"10.1007/s12035-026-06228-6","url":null,"abstract":"<p><p>Cognitive dysfunction is highly prevalent in older adults and severely impairs daily activities and quality of life. Rehabilitation training alleviates aging-related cognitive dysfunction (ARCD); however, the mechanisms underlying differential effects of different training regimens remain poorly understood. Motor training relieves TMAO-triggered neuroinflammation, while cognitive training (CT) improves ARCD via suppression of chronic inflammatory signaling. Cognitive-motor dual-task training (CMDT) yields more obvious cognitive protection than single-mode training, yet the molecular mechanisms accounting for its enhanced protective capacity have not been fully clarified. Thirty 18-month-old male SD rats were subjected to D-galactose injection to establish the ARCD model and randomly divided into five groups (n = 6 per group). Partial model rats received exogenous TMAO administration to verify its neurotoxicity. Animals were treated with CT or CMDT intervention separately. Novel object recognition (NOR) and Morris water maze (MWM) tests were adopted to assess cognitive function; UHPLC-MS/MS, Western blotting and Co-IP were used to detect peripheral and hippocampal TMAO as well as inflammatory protein expression. HT22 cell models were constructed for in vitro validation, with three independent biological replicates set for all molecular measurements. In vivo results showed that CT significantly alleviated cognitive deficits and downregulated hippocampal TXNIP and NLRP3 expression (P < 0.05), without changing circulating or hippocampal TMAO levels (P > 0.05). In contrast, CMDT generated more prominent cognitive improvements and simultaneously reduced TMAO accumulation together with TXNIP overexpression (P < 0.05). In vitro experiments showed that TMAO aggravated D-galactose-induced neuronal senescence and inflammatory activation, which was associated with up-regulation of the TXNIP-NLRP3 inflammatory cascade, and inhibiting TXNIP could reverse such pathological injury. Co-IP assays further showed that TMAO promoted the binding of NLRP3 to ASC, while the caspase-8-ASC binding showed no significant differences across all groups. CMDT exhibits relatively better therapeutic effects against ARCD compared with CT. The present observations reveal that CMDT-related cognitive improvement occurs alongside reduced TMAO accumulation and suppressed TXNIP-NLRP3 inflammatory pathway activation. Combined with our prior MT experimental data, the stronger intervention capacity of CMDT may be related to regulatory effects originating from its cognitive and motor components. This study provides experimental evidence supporting CMDT as a potential rehabilitation strategy for ARCD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative Multi-Omics Analysis Suggests a Proteostasis-Translation-Neuroimmune Axis Underlying Moxifloxacin Associated Cognitive Impairment.","authors":"Hangyu Li, Xinlong Lian, Yuanhui Li, Jingyi Deng, Yuqia Xie, Jie Xie, Dexin Nie, Xiaoxiu Li, Xueqin Huang, Suidong Ouyang","doi":"10.1007/s12035-026-06231-x","DOIUrl":"10.1007/s12035-026-06231-x","url":null,"abstract":"<p><p>Moxifloxacin, a widely used fluoroquinolone antibiotic, has been associated with cognitive impairment, but its molecular mechanisms remain unclear. Here, we applied an integrative multi-omics approach combining network toxicology, transcriptomics, molecular docking, molecular dynamics simulation, and Mendelian randomization to investigate potential mechanisms. We identified 85 overlapping targets linking moxifloxacin to cognitive dysfunction, with HSP90AB1 emerging as a central hub. Molecular docking and molecular dynamics simulations suggested a potential interaction between moxifloxacin and HSP90AB1, which was further supported by biolayer interferometry, yielding an apparent KD of 1.044 ± 0.053 μM. Transcriptomic and enrichment analyses highlighted translation-related pathways and neuroimmune-related signaling, while summary-data-based Mendelian randomization (SMR) analysis implicated APP as a genetically supported candidate component. Experimental validation in BV2 microglial cells showed a reduction in APP protein abundance without a corresponding decrease in APP mRNA, whereas SH-SY5Y cells exhibited a distinct concentration-dependent response. Together, our findings suggest that moxifloxacin-associated cognitive impairment may involve a proteostasis-translation-related-neuroimmune framework, with HSP90AB1 and APP representing candidate molecular components. This study provides a mechanistic framework for fluoroquinolone neurotoxicity and identifies candidate targets for further investigation.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149062632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain-Wide Multi-Trait Genetic Integration Implicates Lysosomal and Metabolic Axes Linking Visual Disturbance and Alzheimer's Disease.","authors":"Zhaocheng Li, Zifei Liu, Yuhang Zhang, Yulin Lei, Yanqing Wang","doi":"10.1007/s12035-026-06211-1","DOIUrl":"10.1007/s12035-026-06211-1","url":null,"abstract":"<p><p>Visual impairment has been proposed as a potentially modifiable risk factor for dementia, including Alzheimer's disease (AD), but the biological mechanisms linking visual disturbance to AD remain unclear. It is unknown whether AD and visual disturbance share specific genetic determinants, how such effects are distributed across brain regions, and whether they converge on discrete molecular pathways that could be targeted for prevention or treatment. Multi-trait analysis of GWAS was applied to summary statistics from large-scale GWAS of AD and a visual disturbance (VD) phenotype, yielding VD-informed AD association statistics (VDAD). Gene-level associations were then mapped across brain tissues by integrating single-tissue and cross-tissue transcriptome-wide association studies, brain proteome-wide association analyses and gene-based tests. A small set of genes (GRN, PVR and RAB29) emerged as consistently associated with both AD and VDAD. A broader panel of genes showed partially overlapping but also phenotype-specific architectures, with PM20D1 and LRRC37A2 more prominent in AD and SLC41A1 and MTCH2 more strongly implicated in VDAD. These signals were anchored to frontal cortical, hippocampal, cerebellar and striatal tissues, suggesting involvement of circuits that integrate visual input with memory, motor control and balance. Network and pathway analyses highlighted a GRN-centered lysosomal axis and metabolic pathways linked to PM20D1 and SLC41A1 as candidate mechanisms bridging visual disturbance and AD risk. These findings support the view that visual disturbance-related AD risk is shaped by a limited set of genes and pathways that are supported across complementary molecular analyses and mapped to distributed brain/CNS reference tissues. These findings generate testable hypotheses for future studies with detailed visual phenotyping.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149062886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into X-linked Dystonia-Parkinsonism and Spinocerebellar Ataxia type 36 Through the Lens of Amyotrophic Lateral Sclerosis/Frontotemporal Dementia.","authors":"Mansee Patel, Soumalya Das, Aditi Pramod Kumari, Amit Kumar","doi":"10.1007/s12035-026-06209-9","DOIUrl":"10.1007/s12035-026-06209-9","url":null,"abstract":"<p><p>The abnormal expansion of repetitive DNA sequences falls within the spectrum of neurological conditions driven by dual pathogenic pathways of RNA toxicity and protein toxicity. Within this spectrum, hexanucleotide repeat disorders (HRDs) represent a rare but important subgroup: C9orf72-amyotrophic lateral sclerosis/frontotemporal dementia (C9orf72-ALS/FTD), X-linked dystonia-parkinsonism (XDP) and spinocerebellar ataxia type 36 (SCA36), unified by the presence of expanded intronic repeats capable of forming non-canonical nucleic acid structures. Despite this shared repeat architecture, they differ in critical molecular and genetic respects: C9orf72-ALS/FTD is hallmarked by TDP-43 aggregation and prominent proteinopathy; SCA36 lacks TDP-43 pathology entirely; and XDP uniquely harbors a SINE-VNTR-Alu (SVA) retrotransposon insertion within the expanded locus and follows an X-linked recessive inheritance pattern. Among these, C9orf72-ALS/FTD is relatively well characterized, with established pathogenic mechanisms including G-quadruplex (G4) formation, dipeptide repeat (DPR) protein toxicity, RNA foci formation, and downstream cellular disruptions. The molecular mechanism underlying SCA36 and XDP remains comparatively less characterized. Given the mechanistic overlap with ALS/FTD, downstream disruptions such as RNA toxicity, mitochondrial dysfunction, impaired DNA repair and proteasomal dysfunction could similarly result from these core molecular processes. However, direct experimental evidence supporting these mechanisms in SCA36 and XDP remains limited. This review compares established, emerging and hypothetical mechanisms across HRDs to distinguish shared pathogenic pathways from disease-specific molecular features. Through horizontal comparison, this review identifies opportunities and limitations for translating ALS/FTD therapeutics to XDP and SCA36, establishing a unified analytical framework for mechanistic research and clinical intervention in rare repeat expansion disorders.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149062157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Symptomatic Rescue or Disease Modification? A Critical Review of Levodopa and Phytochemical Interventions in Caenorhabditis elegans Models of Parkinson's Disease.","authors":"Emre Aktaş, Şeyda Berk","doi":"10.1007/s12035-026-06241-9","DOIUrl":"10.1007/s12035-026-06241-9","url":null,"abstract":"<p><p>Parkinson's disease (PD) is characterised by progressive dopaminergic neurodegeneration and alpha-synuclein (α-syn) aggregation, with levodopa remaining the gold-standard symptomatic therapy despite its inability to halt disease progression or prevent levodopa-induced dyskinesia (LID). Caenorhabditis elegans has emerged as a highly tractable model for mechanistic PD research owing to its conserved dopaminergic pathways, optical transparency, rapid lifecycle, and suitability for high-throughput pharmacological screening. This review critically examines the pharmacological effects of levodopa in C. elegans PD models across locomotor behaviour, α-syn aggregation, lifespan, and dyskinesia-related phenotypes, while comparing these findings with phytochemicals evaluated in analogous experimental systems. Levodopa consistently restored dopamine-dependent locomotor deficits but failed to substantially reduce α-syn aggregation or extend lifespan, recapitulating the clinical dissociation between symptomatic motor rescue and persistent neurodegeneration. In contrast, phytochemicals, including Frondoside A, hydroxytyrosol/Hidrox®, Neurogrit Gold, Mucuna pruriens extract, quercetin, and quercetin nanoemulsions, demonstrated broader mechanistic profiles involving antioxidant responses, mitophagy, proteostasis, and dopaminergic neuroprotection. The available evidence suggests that phytochemicals are best regarded not as replacements for levodopa but as candidate adjuncts that, in preclinical worm models, appear to act on upstream pathological processes; whether this translates into genuine complementarity in vivo remains a hypothesis requiring direct testing. The central argument advanced here is methodological rather than pharmacological: C. elegans is currently the only PD model in which symptomatic motor rescue and α-synuclein pathology can be quantified simultaneously in the same living animal, and this dissociation provides a measurable framework for defining what an adjunctive compound would need to achieve. On this basis, levodopa is proposed as a mandatory positive control for future C. elegans phytochemical screening. Critical translational limitations-including the absence of a blood-brain barrier in C. elegans, phytochemical bioavailability constraints, and uncertainty regarding the relationship between aggregate reduction and true neuroprotection-are also discussed.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149062772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral IL-17 Triggers, and anti-IL-17 Treatment Prevents, Neuroinflammation and Alterations in Neurotransmission in Hippocampus and Cognitive Impairment in Hyperammonemic Rats.","authors":"Yaiza M Arenas, Marta Llansola, Gergana Mincheva, Carmina Montoliu, Vicente Felipo","doi":"10.1007/s12035-026-06229-5","DOIUrl":"10.1007/s12035-026-06229-5","url":null,"abstract":"<p><p>Patients with liver cirrhosis who develop minimal hepatic encephalopathy (MHE) show mild cognitive impairment associated with increased peripheral inflammation, including elevated interleukin-17 (IL-17). In animal models, this inflammation promotes neuroinflammation and disrupts glutamatergic neurotransmission in the hippocampus, contributing to cognitive deficits. This study investigated whether IL-17 is directly involved in cognitive impairment in hyperammonemic rats and explored the mechanisms involved. Hyperammonemic rats received intravenous anti-IL-17 treatment at days 3-5 after induction of hyperammonemia. Cognitive assessment and blood-brain barrier integrity, neuroinflammation, and glutamatergic neurotransmission in the hippocampus were performed after four weeks. Increased peripheral IL-17 activated its receptor in endothelial cells, enhancing NADPH oxidase activity and increasing Myosin light chain kinase (MLCK) levels. This reduced the tight junction proteins occludin and ZO-1, weakening the blood-brain barrier and facilitating immune cell infiltration and IL-17 entry into the hippocampus. Consequently, microglia became activated, increasing TNFα and IL-1β levels and altering membrane expression of glutamate receptors, leading to cognitive impairment. Blocking IL-17 prevented these pathological changes and produced sustained protection against cognitive deficits. These findings support a role of IL-17 in early transmission of peripheral inflammation into the brain initiating hippocampal neuroinflammation and cognitive impairment in MHE and propose anti-IL-17 therapies for MHE.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149062597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"West Nile Virus Exploits miR-155-5p-Mediated Regulation of TRIM32-IκBα Axis to Evade NF-κB-Mediated Innate Immune Responses in Human Microglial Cells.","authors":"Vishal Keshri, Sunit K Singh","doi":"10.1007/s12035-026-06233-9","DOIUrl":"10.1007/s12035-026-06233-9","url":null,"abstract":"<p><p>West Nile virus (WNV) is a neurotropic virus, having a single-stranded, positive-sense RNA genome belonging to the Flaviviridae family. WNV infection in the brain is associated with many neurological sequelae. Microglia are brain macrophages that respond to pathogenic breaches and eliminate threats. However, WNV is reported to evade cellular challenges and cause infection in the brain. In this study, we explored an underlying strategy by which WNV suppresses inflammation in microglial cells by increasing cellular microRNA-155-5p and dampening nuclear factor of kappa light-chain enhancer of activated B cells (NF-κB) signaling via tripartite motif-containing protein 32 (TRIM32). NF-κB is a crucial transcription factor involved in the production of pro-inflammatory cytokines and mediating cellular response. We observed increased expression of miR-155-5p in WNV-infected human microglial cells. The miR-155-5p-mediated regulation of TRIM32 and downstream NF-κB signaling was validated by miR-155-5p overexpression and knockdown in HMC3 cells. Increased miR-155-5p expression led to decreased TRIM32 expression. The decrease in TRIM32 sequestered the localization of inhibitor of nuclear factor of kappa light chain enhancer of activated B-cells, alpha (IκBα), and reduced its phosphorylation-mediated degradation. Consequently, resulting in decreased phosphorylation of NF-κB and decreased production of inflammatory cytokines. The protein expression patterns of TRIM32, p-IκBα, IκBα, p-NF-κB, NF-κB, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were assessed by immunoblotting. This study demonstrates that WNV modulates host cellular machinery by dysregulating miR-155-5p, thereby suppressing the host inflammatory response in human microglial cells.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149062824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}