Neuroreport最新文献

{"title":"Glutaredoxin-1 attenuates transactive response DNA-binding protein 43-induced neurotoxicity by suppressing oxidative stress and transactive response DNA-binding protein 43 aggregation.","authors":"Ji Min Lee, Eugene Bok, Sang Ryong Kim, Jaekwang Kim","doi":"10.1097/WNR.0000000000002266","DOIUrl":"10.1097/WNR.0000000000002266","url":null,"abstract":"<p><strong>Objective: </strong>Cytoplasmic aggregation of transactive response DNA-binding protein 43 (TDP-43) represents pathological hallmarks of TDP-43 proteinopathies. Accumulating evidence indicates that oxidative stress plays a pivotal role in these disorders by promoting TDP-43 aggregation and subsequent neurotoxicity. Glutaredoxin-1 (Grx1) is a key antioxidant enzyme that maintains cellular redox homeostasis. In this study, we investigated the role of Grx1 in TDP-43 proteinopathy.</p><p><strong>Methods: </strong>We examined the effects of Grx1 in neuro-2a cells expressing human wild-type TDP-43 (N2a-hTDP-43), a cellular model of TDP-43 proteinopathy characterized by increased oxidative stress, TDP-43 aggregation, and neurotoxicity.</p><p><strong>Results: </strong>In N2a-hTDP-43 cells, Grx1 expression was increased in parallel with elevated oxidative stress. Increasing Grx1 significantly suppresses intracellular oxidative stress and cytoplasmic TDP-43 aggregation in N2a-hTDP-43 cells. Notably, increasing Grx1 significantly reduces cleaved caspase-3 levels in N2a-hTDP-43 cells, indicating reduced neurotoxicity.</p><p><strong>Conclusion: </strong>Collectively, our findings demonstrate that Grx1 attenuates neurotoxicity by suppressing oxidative stress and TDP-43 aggregation, highlighting its potential as a therapeutic target for TDP-43 proteinopathies.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"319-323"},"PeriodicalIF":2.1,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of dexmedetomidine-induced cerebral protection following ischemic brain injury via the brain-derived neurotrophic factor-tyrosine kinase receptor B pathway.","authors":"Alimujiang Simayi, Li Qu, Xiao-Li Wang, Wan-Ying Cao, Xuan Zhao, Gui-Ping Xu","doi":"10.1097/WNR.0000000000002256","DOIUrl":"10.1097/WNR.0000000000002256","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the protective effects of dexmedetomidine on cerebral ischemia-reperfusion injury through the activation of the brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling pathway.</p><p><strong>Methods: </strong>This study utilized hippocampal neuronal oxygen-glucose deprivation/reoxygenation (OGD/R) models and rat middle cerebral artery occlusion models, with dexmedetomidine intervention.</p><p><strong>Results: </strong>Compared with the sham-operated group, the model group rats exhibited a significant increase in Zea-Longa scores, a marked prolongation of the escape latency, a notable reduction in the number of platform crossings, a significant increase in the percentage of cerebral infarct size, and a marked decrease in the expression of BDNF, TrkB, and Bcl-2 proteins and mRNA ( P  < 0.05). The dexmedetomidine group showed significantly better outcomes in all above parameters compared to the model group. Compared with the control group, the OGD/R group exhibited a reduction in hippocampal neuronal cell viability, a significant increase in apoptosis rate, elevated expression of Bax and C-caspase-3 proteins, a marked decrease in Bcl-2 protein levels, and a significant reduction in the expression of BDNF and TrkB proteins and mRNA ( P  < 0.05).</p><p><strong>Conclusion: </strong>Dexmedetomidine exerts significant neuroprotective effects by activating the BDNF/TrkB signaling pathway, thereby alleviating ischemic brain injury.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"297-307"},"PeriodicalIF":2.1,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircOGDH promotes oxygen-glucose deprivation/reoxygenation-induced neuron injury by targeting the miR-195-5p/brain-specific angiogenesis inhibitor 1-associated protein 2 axis.","authors":"Ruibin Zheng, Zhanhai Huang, Hongchuan Zhou, Liguo Zhang","doi":"10.1097/WNR.0000000000002261","DOIUrl":"10.1097/WNR.0000000000002261","url":null,"abstract":"<p><strong>Objective: </strong>Stroke remains a major cause of disability and death worldwide, with inflammation and oxidative stress that play important roles in its pathogenesis. This study aimed to explore the role of circOGDH in stroke and its mechanism of action.</p><p><strong>Methods: </strong>SH-SY5Y cells were transfected with circOGDH, miR-195-5p, and brain-specific angiogenesis inhibitor 1-associated protein 2 (BAP2) vectors, and oxygen-glucose deprivation/reoxygenation (OGD/R) models were established. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to assess cell proliferation and flow cytometry was used to measure reactive oxygen species (ROS) activity and apoptotic rates. Inflammatory factor ELISAs were performed. Superoxide dismutase activity and malondialdehyde concentration were measured using assay kits. Luciferase reporters were used to analyze molecular binding.</p><p><strong>Results: </strong>CircOGDH or BAP2 knockdown or miR-195-5p overexpression inhibited the effects of OGD/R on SH-SY5Y cells, including decreased proliferation and superoxide dismutase activity, as well as increased apoptosis, ROS production, malondialdehyde concentration, and inflammatory factor levels. In SH-SY5Y cells, circOGDH targeted miR-195-5p to upregulate BAP2 expression. miR-195-5p inhibition or BAP2 overexpression eliminated circOGDH knockdown-elicited protection of SH-SY5Y cells against OGD/R.</p><p><strong>Conclusion: </strong>CircOGDH aggravates OGD/R-caused SH-SY5Y cell injury and promotes inflammatory factor secretion and oxidative stress by targeting miR-195-5p to upregulate BAP2 expression.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"277-285"},"PeriodicalIF":2.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147531274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of mirror activity by transcranial direct current stimulation of the supplementary motor area.","authors":"Akihiro Matsuura, Manami Hada, Yuji Nishioka, Futoshi Mori","doi":"10.1097/WNR.0000000000002262","DOIUrl":"10.1097/WNR.0000000000002262","url":null,"abstract":"<p><strong>Objective: </strong>We investigated whether transcranial direct current stimulation (tDCS) applied to the supplementary motor area (SMA) modulates mirror activity induced by transcranial magnetic stimulation (TMS) during a unilateral precision pinch task.</p><p><strong>Methods: </strong>Healthy subjects performed a left-hand precision pinch task during the delivery of single-pulse TMS to the left primary motor cortex (M1) to evoke mirror activity in the right hand. Anodal, cathodal, and sham tDCS were applied over the SMA via a randomized crossover design. Motor-evoked potentials recorded from the right first dorsal interosseous muscle were used to quantify mirror activity. Pinch performance variability was evaluated.</p><p><strong>Results: </strong>Although anodal tDCS tended to increase mirror activity, the effect did not differ significantly from that of sham tDCS. In contrast, cathodal tDCS significantly reduced mirror activity compared with the effects of sham and anodal tDCS. Pinch performance variability did not differ among the tDCS conditions, indicating that mirror activity changed independently of motor performance. Resting motor-evoked potential amplitudes elicited by single-pulse TMS were not significantly altered by tDCS targeting the SMA.</p><p><strong>Conclusion: </strong>Mirror activity is modulated by SMA excitability. The findings indicate that cathodal tDCS applied to the SMA reduces mirror activity, potentially through alterations in cortical network interactions between the SMA and M1.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"286-289"},"PeriodicalIF":2.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered gray matter volume in major depressive disorder patients with psychomotor retardation.","authors":"Yiyun Wang, Lijin Yuan, Xiaoyun Luo, Jigang Lian, Yun Zhu, Zonglin Shen","doi":"10.1097/WNR.0000000000002263","DOIUrl":"10.1097/WNR.0000000000002263","url":null,"abstract":"<p><strong>Background: </strong>Psychomotor retardation (PMR) is a clinically significant but under-investigated neuropsychiatric manifestation of major depressive disorder (MDD). Its neuroanatomical features remain poorly understood. This study aims to examine differences in gray matter volume (GMV) alterations between MDD patients with and without PMR.</p><p><strong>Methods: </strong>The study enrolled 107 first-episode, treatment-naïve MDD patients (diagnosed per DSM-IV criteria) and 112 age- and sex-matched healthy controls. Participants were divided into two clinical subgroups based on the retardation factor score of the 17-item Hamilton Depression Rating Scale: an MDD with retardation (MDD-WR) group (score ≥ 8, n  = 51) and an MDD without retardation (MDD-WoR) group (score < 8, n  = 56). Structural MRI scans were obtained for all participants.</p><p><strong>Results: </strong>Compared with healthy controls, the MDD-WR group showed significantly smaller GMV in the bilateral posterior cerebellum and left calcarine gyrus. In contrast, the MDD-WoR group demonstrated larger GMV in the left postcentral gyrus (PoCG) and right angular gyrus. Among all of the MDD patients, patients of the MDD-WR group had smaller GMV in the right PoCG, right superior frontal gyrus, and left olfactory bulb compared with the MDD-WoR group.</p><p><strong>Conclusion: </strong>Our findings identify distinct neuroanatomical patterns of GMV changes in MDD patients with PMR compared with those without PMR. This provides novel insights into the neural basis of PMR in MDD.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"290-296"},"PeriodicalIF":2.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13061376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147531285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opposite modulation of sensorimotor rhythms in 3-8 years children by passive hand movement and hand movement observation.","authors":"Vladimir Lipatov, Anna Rebreikina, Olga Sysoeva","doi":"10.1097/WNR.0000000000002254","DOIUrl":"10.1097/WNR.0000000000002254","url":null,"abstract":"<p><strong>Objective: </strong>Sensorimotor rhythms can be potential markers of atypical child development; however, many paradigms used in research of sensorimotor rhythms are difficult to use in children with developmental disabilities. In this paper, we explored two experimental paradigms for sensorimotor rhythms investigation that can potentially be used in children with developmental disorders.</p><p><strong>Methods: </strong>Electroencephalography was recorded in typically developing children aged 3-8 years ( N  = 58), during the inclusive passive hand movement paradigm (PHM), the hand movement observation on video paradigm (VWH), and control condition (video with fractals). The difference in the mu-rhythm power was analyzed between experimental and control conditions at the central electrodes (C3 and C4).</p><p><strong>Results: </strong>The PHM causes significant desynchronization of the mu rhythm in the 6-13 and 13-30 Hz ranges, predominantly in the right motor region, suggesting activation of motor programs. In contrast, the VWH paradigm caused an increase in the mu rhythm in the 6-13 Hz range relative to the control condition, predominantly over left motor cortex, suggesting deactivation or underdevelopment of motor representation in children of such age during hand movement observation.</p><p><strong>Conclusion: </strong>While PHM consistently elicits mu rhythm desynchronization, observation of hand movement could induce the opposite effect, which needs further investigation.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"215-221"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of 75NTR extracellular domain in rotenone-induced Parkinson's disease cell models.","authors":"Yifei You, Anyan Ren, Nan Wang, Fang Chen, Xianzhi Wang, Chen Li, Hongcai Wang","doi":"10.1097/WNR.0000000000002258","DOIUrl":"10.1097/WNR.0000000000002258","url":null,"abstract":"<p><strong>Objective: </strong>While the p75 neurotrophin receptor (p75NTR) is critically implicated in the aggregation of α-synuclein (α-syn), a defining pathological hallmark of Parkinson's disease, the distinct functional contributions of its structural domains remain largely unresolved.</p><p><strong>Methods: </strong>To investigate this, we employed a rotenone-induced cellular Parkinson's disease model utilizing SH-SY5Y neuroblastoma cells transfected with plasmids encoding specific p75NTR truncation mutants.</p><p><strong>Results: </strong>Overexpression of a mutant representing the p75NTR extracellular domain (HA-p75Δ151, lacking residues 277-427) significantly exacerbated both α-syn expression levels and its aggregation phenotype. This effect is potentially attributable to the aberrant activation of caspase-1. Conversely, unlike full-length p75NTR which enhanced α-syn ubiquitination, the HA-p75Δ151 truncation failed to modulate ubiquitination dynamics. Furthermore, expression of this extracellular domain fragment induced cell cycle dysregulation and promoted cell death.</p><p><strong>Conclusion: </strong>These findings delineate the p75NTR extracellular domain-induced α-syn proteotoxic stress. This domain-specific mechanism advances our understanding of Parkinson's disease pathogenesis and highlights the therapeutic potential of targeting specific p75NTR domains.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"247-257"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-766-3p regulates neurological deficits and inflammation after cerebral hemorrhage by targeting bradykinin receptor B2.","authors":"Bin Han, Yu Hao, Yang Lin, Min Yang, Fengyi Che","doi":"10.1097/WNR.0000000000002260","DOIUrl":"10.1097/WNR.0000000000002260","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to clarify the protective effect of miR-766-3p on brain injury caused by intracerebral hemorrhage (ICH), and to reveal the mechanisms by which it regulates neural function, neuroinflammation, and brain edema.</p><p><strong>Methods: </strong>An ICH rat model was constructed and PC12 cells were treated with hemin to simulate neuronal injury. Quantitative reverse transcription PCR was used to detect the expression of miR-766-3p and inflammatory factors. Cell counting kit-8 and flow cytometry were used to assess cell viability and apoptosis. Brain edema was evaluated by the dry-wet method. Neurological function was assessed through the Garcia score, forelimb placement test, and corner turn test. The dual-luciferase reporter assay and RNA immunoprecipitation were employed to validate the targeting relationship between miR-766-3p and bradykinin receptor B2 (BDKRB2).</p><p><strong>Results: </strong>The expression of miR-766-3p was significantly downregulated in the brain tissue surrounding the hematoma and PC12 cells. Overexpression of miR-766-3p increased the survival rate of neuronal cells, inhibited apoptosis, and reduced the release of inflammatory factors. In vivo experiments demonstrated that this intervention measure improved neurological function scores and placement rate of the forelimbs while alleviating turning disorders, brain edema, and neuroinflammation. miR-766-3p directly targets BDKRB2 and inhibits its expression. Overexpression of BDKRB2 completely reversed the neuroprotective effects of miR-766-3p.</p><p><strong>Conclusion: </strong>miR-766-3p alleviates neuroinflammation, cerebral edema, and neuronal damage caused by ICH by targeting and inhibiting BDKRB2.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"265-275"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acupoint catgut embedding ameliorates laparotomy-induced cognitive decline in aged mice by restoring gut microbiota.","authors":"Lijuan Zhang, Xianzhang Zeng, Can Ma, Yuting Wei, Weina Wang, Tianhua Liu, Wenzhi Li","doi":"10.1097/WNR.0000000000002255","DOIUrl":"10.1097/WNR.0000000000002255","url":null,"abstract":"<p><strong>Background: </strong>Postoperative cognitive dysfunction (POCD), a common neurological complication in elderly patients, significantly impairs recovery. Emerging evidence suggests the gut microbiota is involved in its pathogenesis. This study aimed to determine whether acupoint catgut embedding (ACE) could alleviate POCD by modulating the gut microbiota in aged mice after laparotomy.</p><p><strong>Methods: </strong>Eighteen-month-old male C57BL/6J mice underwent laparotomy on day 8 (excluding the Sham group). The ACE group received ACE treatment, while the anesthesia and surgery group served as surgical controls. The fecal microbiota transplantation (FMT)-ACE and FMT-AS groups received FMT from corresponding donors. Additional groups received oral indole-3-propionic acid (IPA) or vehicle-treated surgery. Hippocampal inflammation and blood-brain barrier proteins were assessed on day 9; cognitive function and intestinal markers on day 15.</p><p><strong>Results: </strong>Cognitive function was significantly improved in the ACE, FMT-ACE, and IPA groups. ACE and FMT-ACE treatments specifically elevated fecal g-Clostridia_UCG-014 abundance and serum IPA levels. These changes were accompanied by suppressed hippocampal toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling and proinflammatory cytokines [tumor necrosis factor alpha, interleukin (IL)-1β], together with elevated tight junction proteins (occludin, claudin-5). Furthermore, colonic aryl hydrocarbon receptor (AhR) and IL-22 were upregulated, while serum lipopolysaccharide and diamine oxidase were reduced. Accordingly, IPA treatment mirrored the key anti-inflammatory and barrier-protective effects.</p><p><strong>Conclusion: </strong>ACE alleviates POCD probably by modulating gut microbiota, specifically increasing g-Clostridia_UCG-014 abundance and metabolite IPA. These effects are potentially mediated by dual pathways: (a) suppression of neuroinflammation via TLR4/NF-κB signaling, and (b) enhancement of gut barrier integrity via AhR/IL-22 axis. Our findings highlight the therapeutic potential of ACE in targeting the gut-brain axis for POCD management.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"222-235"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pretreatment with a histone deacetylase inhibitor, sodium butyrate, potentiates the sustained expression of myelin-associated and neurotrophic genes in cultured Schwann cells.","authors":"Yuan Ding, Taichi Nishio, Kaori Tsutsumi, Yuichiro Oka, Hiroshi Maejima","doi":"10.1097/WNR.0000000000002259","DOIUrl":"10.1097/WNR.0000000000002259","url":null,"abstract":"<p><strong>Objectives: </strong>Schwann cells have therapeutic potential for central nervous system repair, but their limited posttransplant survival remains a major challenge. Because histone deacetylase inhibitors (HDACIs) can enhance genes involved in myelination potential and neurotrophic support, this study investigated whether sodium butyrate (NaB), an HDACI, promotes the expression and sustained regulation of myelin‑associated and neurotrophic genes in cultured Schwann cells.</p><p><strong>Methods: </strong>Cultured Schwann cells were treated with 1 or 10 mM NaB for either 48 h (prolonged treatment) or 24 h followed by reagent washout (transient treatment). Expression of myelin-associated genes, neurotrophic factors, and apoptosis marker were quantified using quantitative reverse transcription PCR. Cell viability was assessed via Cell Counting Kit-8 assay.</p><p><strong>Results: </strong>Prolonged treatment with NaB increased the expression of myelin-associated genes ( Mbp and Mpz ) and neurotrophic genes ( Igf-1 and Gdnf ). Furthermore, transient NaB treatment increased these gene expressions for up to 24 h after reagent washout and attenuated NaB‑induced apoptosis. Specifically, transient treatment with a high dose of NaB strongly sustained the enhanced expression of the myelin marker, Mpz .</p><p><strong>Conclusion: </strong>Transient pre‑treatment with NaB enhanced and sustained the expression of certain key myelin‑associated and neurotrophic genes in Schwann cells while reducing cytotoxic effects. These findings suggest a potential strategy to improve certain Schwann cell functions and support further investigation of HDACI‑based approaches in regenerative therapy.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"258-264"},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}