Brain Research Bulletin最新文献

{"title":"Nerol ameliorates cognitive dysfunction in vascular dementia rats by inhibiting mitochondrial oxidative stress and reducing hippocampal senescence.","authors":"Jing Yang, Qian-Qian Niu, Na Liu, Bo Wang, Ya-Jun Shen, De-Sheng Liu, Xiao-Wen Li, Mo-Li Zhu, Qian-Qian Wang, Ya-Qi Guo","doi":"10.1016/j.brainresbull.2026.111753","DOIUrl":"10.1016/j.brainresbull.2026.111753","url":null,"abstract":"<p><p>Vascular dementia (VaD) is a neurodegenerative disease caused by chronic cerebral hypoperfusion and is mainly characterized by cognitive dysfunction. This study established a VaD rat model using permanent bilateral common carotid artery occlusion (2-VO), administered different doses of nerol for 8 weeks, and evaluated cognitive function using the Morris water maze and Y-maze tests, while systematically analyzing hippocampal neuronal structure, senescence, mitochondrial function, oxidative stress, and apoptosis-related changes. The results showed that nerol improved spatial learning, memory ability, and exploratory behavior in VaD rats, and alleviated hippocampal neuronal structural damage and dendritic degeneration. At the same time, nerol reduced the number of senescence-associated β-galactosidase-positive and TUNEL-positive cells and downregulated the expression of p53 and p21. Mechanistically, nerol inhibited NOX2/NOX4-mediated reactive oxygen species production, enhanced antioxidant capacity, stabilized mitochondrial membrane potential, and suppressed DRP1/FIS1-mediated abnormal mitochondrial fission, thereby potentially attenuating oxidative stress-related neuronal senescence and apoptosis and improving cognitive function. These findings provide experimental evidence supporting the potential therapeutic value of nerol in vascular dementia.</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"111753"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146096675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional magnetic resonance-based analysis of dynamic functional connectivity in patients with olfactory impairment in Parkinson's disease.","authors":"Fangling He, Huihua Liu","doi":"10.1016/j.brainresbull.2026.111750","DOIUrl":"10.1016/j.brainresbull.2026.111750","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this research is to utilize resting-state functional magnetic resonance imaging (rs-fMRI), combined with sliding-window and cluster analysis methods. To identify alterations in functional connectivity (FC) patterns in patients with Parkinson's disease who exhibit olfactory dysfunction prior to the onset of motor symptoms, compared to healthy individuals.This method is intended to improve capabilities for the early detection of PD.</p><p><strong>Materials and methods: </strong>We recruited fifteen individuals from three distinct groups: PD patients with no or mild olfactory dysfunction (PD-N/MH), those with severe olfactory dysfunction, and healthy controls (HC). We gathered and analyzed resting-state fMRI data to examine dynamic FC across these groups, subsequently conducting a thorough statistical evaluation.</p><p><strong>Results: </strong>Our cluster analysis identified two unique states of brain network connections across the groups. Notably, the subgroup with PD exhibited a more frequent occurrence and extended duration in state 1, along with reduced state transitions. Notably, the severity of olfactory dysfunction was significantly correlated with increased durations and frequencies in state 1 (P ＜0.05).</p><p><strong>Conclusion: </strong>These observations underscore the significant relationship between state 1 connectivity patterns and olfactory impairment in PD patients. The discovery that PD patients with Parkinson's disease (PD) \"linger\" in the sparsely connected state 1 provides a dynamic functional correlate of the progressive pathology that initially affects olfaction. Dynamic functional connectivity analysis successfully distinguished PD patients from healthy controls even prior to the onset of motor symptoms, suggesting its potential as a neuroimaging biomarker for Parkinson's disease. Consequently, this method may facilitate early identification, timely intervention, and improved clinical management of PD by providing an early warning signal before motor symptom--based diagnosis, thereby potentially delaying disease progression and alleviating the burden on patients, families, and society.</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"111750"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kininogen-1 modulates cGMP-PKG signaling to alleviate inflammatory neuronal injury in intracerebral hemorrhage","authors":"Yuan Wang ,&nbsp;Jing Zhao ,&nbsp;Kaijie Wang ,&nbsp;Shuwei Wang ,&nbsp;Jie Li ,&nbsp;Chaopeng Xu ,&nbsp;Haoyu Wang ,&nbsp;Jianzhong Cui","doi":"10.1016/j.brainresbull.2026.111740","DOIUrl":"10.1016/j.brainresbull.2026.111740","url":null,"abstract":"<div><h3>Objective</h3><div>Although the pathological mechanisms underlying intracerebral hemorrhage (ICH) have been widely explored, the contribution of kininogen-1 (Kng1) to inflammation-associated neuronal damage has not been fully elucidated. This study was designed to investigate the functional involvement of Kng1 and the cyclic guanosine monophosphate (cGMP)–protein kinase G (PKG) signaling cascade in inflammation-driven neuronal injury following cerebral hemorrhage.</div></div><div><h3>Methods</h3><div>Bioinformatics analyses based on Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases were employed to identify Kng1 and the cGMP-PKG pathway as key candidates. An in vivo ICH model was generated by intracerebral injection of autologous blood, while an in vitro hemorrhagic injury model was established by treating neuronal cells with hemoglobin chloride. Levels of inflammatory mediators and gene expression were determined using enzyme-linked immunosorbent assay, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, and reverse transcription-quantitative polymerase chain reaction. Neurological impairment and cerebral edema were evaluated through behavioral deficit scoring and brain water content analysis, respectively.</div></div><div><h3>Results</h3><div>Kng1 protein levels were markedly increased in the serum of patients with ICH as well as in experimental hemorrhage models, and this elevation was closely associated with enhanced neuroinflammatory responses. Suppression of Kng1 expression significantly alleviated neurological dysfunction, reduced cerebral edema, mitigated inflammatory activation, and limited neuronal apoptosis in ICH rats. Further mechanistic investigations demonstrated that Kng1 modulates the cGMP-PKG signaling axis, as pharmacological stimulation of cGMP or PKG reversed the protective effects induced by Kng1 silencing. Consistent findings from both animal and cellular rescue experiments indicated that Kng1 aggravates neuronal injury after ICH by activating cGMP-PKG-dependent inflammatory signaling pathways.</div></div><div><h3>Conclusion</h3><div>Kng1 regulates the cGMP-PKG signaling pathway, influencing neuronal cell injury induced by the inflammatory response in ICH conditions. These findings suggest Kng1 as a potential therapeutic target for mitigating ICH-induced neuronal damage.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"235 ","pages":"Article 111740"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adaptive immune dysregulation in depression: Cross-species evidence of CD4+ T cell dysfunction and pro-inflammatory pathway activation","authors":"Liekui Hu ,&nbsp;Zhaozhi Qiu ,&nbsp;Zhifu Ai ,&nbsp;Rui Liu ,&nbsp;Bike Zhang ,&nbsp;Huizhen Li","doi":"10.1016/j.brainresbull.2026.111752","DOIUrl":"10.1016/j.brainresbull.2026.111752","url":null,"abstract":"<div><div>The association between central adaptive immunity and depression remains highly debated. In this study, we systematically assessed the role of adaptive immune mechanisms in depression using a mouse model of chronic unpredictable mild stress (CUMS) and the peripheral blood of patients with depression. The behavioral results demonstrated that the CUMS mice exhibited typical depression-like behaviors. Subsequent transcriptomic analysis of the hippocampus identified 203 differentially expressed genes (DEGs), of which CD4 expression was significantly downregulated. Furthermore, DEGs were enriched in the tumor necrosis factor (TNF) and interleukin (IL)-17 signaling pathways. Validation experiments further corroborated the hypothesis that the CD4 gene in the hippocampal region of CUMS mice was reduced in parallel with the protein levels. Immunocorrelation assays revealed a decrease in intercellular cell adhesion molecule-1 expression in the hippocampus, along with an increase in vascular cell adhesion molecule-1 expression. These changes were accompanied by cytokine level disruption in CUMS mice. A total of 391 DEGs were identified in the transcriptome sequencing of peripheral blood CD4⁺T cells from patients with depression using the Gene Expression Omnibus database. These DEGs were significantly associated with the PI3K-AKT, IL-17, and TNF signaling pathways. Immune checkpoint analysis revealed elevated PDCD1 and decreased TIGIT expression in CD4⁺T cells of the patients. The integration of animal models and clinical data revealed a convergent pattern of findings, indicating CD4⁺ T-cell dysfunction and the activation of pro-inflammatory pathways as immune features shared across species in depression. This provides a novel rationale for targeted immunomodulatory treatment of depression.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"235 ","pages":"Article 111752"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146090181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dendrobine attenuates postoperative cognitive dysfunction by inhibiting Runx1-mediated NF-κB signaling pathway","authors":"Dong Ji ,&nbsp;Qingyu Sun ,&nbsp;Chengcheng Zhang ,&nbsp;Mingyi Zang ,&nbsp;Wei Xiao ,&nbsp;Jie Liu ,&nbsp;Xiaohua Fan ,&nbsp;Hongbing Wang","doi":"10.1016/j.brainresbull.2026.111746","DOIUrl":"10.1016/j.brainresbull.2026.111746","url":null,"abstract":"<div><h3>Background</h3><div>Postoperative cognitive dysfunction (POCD) in older adults is strongly linked to neuroinflammation driven by microglial activation and NF-κB signaling. Runx1 has emerged as an upstream regulator of NF-κB, but its role in POCD is unknown. Dendrobine, a sesquiterpenoid alkaloid from Dendrobium species, exhibits anti-inflammatory and neuroprotective activity.</div></div><div><h3>Methods</h3><div>POCD was induced in aged C57BL/6 mice via sevoflurane anesthesia combined with exploratory laparotomy. Dendrobine (10 or 20 mg/kg) was administered, and cognitive outcomes were evaluated by Morris Water Maze and Novel Object Recognition. RNA sequencing, Western blotting, immunofluorescence, and in vitro microglia-neuron co-culture systems were employed to investigate inflammatory responses, apoptosis, synaptic plasticity, and signaling pathway activation. Functional roles of Runx1 were validated via siRNA knockdown, pharmacological inhibition (Ro5–3335), and overexpression in BV2 cells.</div></div><div><h3>Results</h3><div>Dendrobine improved spatial and recognition memory in POCD mice, reduced hippocampal microglial activation, proinflammatory cytokine expression (TNF-α, IL-1β, IL-6), and neuronal apoptosis while enhancing synaptic protein levels (BDNF, PSD95, SYN1). Transcriptomic and KEGG analyses revealed suppression of NF-κB signaling by dendrobine, with Runx1 identified as an upstream modulator. Dendrobine downregulated Runx1 expression in vivo and in vitro. Runx1 inhibition enhanced dendrobine’s anti-inflammatory effects, whereas RUNX1 overexpression abolished them.</div></div><div><h3>Conclusion</h3><div>Dendrobine ameliorates POCD by inhibiting the Runx1/NF-κB signaling pathway, suppressing neuroinflammation, promoting synaptic resilience, and preventing neuronal apoptosis. Runx1 appears to act as a key upstream mediator of NF-κB signaling in POCD. Targeting the Runx1/NF-κB axis represents a promising strategy for perioperative neuroprotection.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"235 ","pages":"Article 111746"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146090717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treadmill exercise attenuates CUMS-induced depressive behaviors by modulating the UPRmt via the Nrf2/Keap1 pathway","authors":"Yang Wang ,&nbsp;Mingshi Peng ,&nbsp;Tongxi Zhou ,&nbsp;Juncheng Si ,&nbsp;Yuwen Shangguan ,&nbsp;Jingfeng Wang ,&nbsp;Siyun Lei ,&nbsp;Li Li","doi":"10.1016/j.brainresbull.2026.111738","DOIUrl":"10.1016/j.brainresbull.2026.111738","url":null,"abstract":"<div><h3>Introduction</h3><div>Depression is a very common brain disorder worldwide. It is associated with damaging behaviors such as self-harm and suicide that hurt the brain and body. Mitochondrial dysfunction and dysregulation of the mitochondrial unfolded protein response (UPRmt) are increasingly seen as playing a key role in chronic stress-induced pathophysiology of depression. Aerobic exercise is a very effective non-pharmacological intervention, however, the specific mechanisms of how it modifies hippocampal UPRmt is poorly understood. This effect may be attributed to the Nrf2/Keap1 pathway, a master regulator of cellular antioxidant defense that mediates exercise-induced neuroprotection. This study aimed to investigate whether treadmill exercise modulates UPRmt dysregulation in CUMS-induced depressive mice by activating the hippocampal Nrf2/Keap1 signaling pathway, thereby ameliorating mitochondrial dysfunction and depression-like behaviors.</div></div><div><h3>Methods</h3><div>Male C57BL/6 J mice were subjected to a chronic unpredictable model of stress for the induction of a depression model which through exercise on a treadmill for 6 weeks was tested for therapeutic effects. Behaviors consistent with a model of depressive behavior were assessed by OFT, SPT, and TST. Hippocampal mitochondrial function was assessed by transmission electron microscopy, flow cytometry, biochemical, and ELISA. Oxidative stress markers were assessed with biochemical kits and ELISA. The mRNA and protein levels of key markers in the Nrf2/Keap1 pathway and UPRmt were analyzed using RT-qPCR, Western blotting, and immunofluorescence. Pathway dependence was determined using the Nrf2 inhibitor, ML385 and the Nrf2 activator Bardoxolone methyl.</div></div><div><h3>Results</h3><div>The six-week treadmill exercise program significantly reduced depression-like behaviors (e.g., anxiety-like behaviors, anhedonia, and behavioral despair), restored mitochondrial functions (mitochondrial cristae morphology, Δψm, ATP, and ROS levels) and eliminated oxidative stress (SOD, T-AOC, and MDA levels). Moreover, treadmill exercise significantly increased the expression of proteins in the Nrf2/Keap1 pathway (Nrf2, Keap1, NQO1, and HO-1), which attenuated CUMS-induced UPRmt markers (HSP60, ClpP, HSP70, LONP1, and ATF5) and the associated stress transcription factor CHOP.</div></div><div><h3>Conclusion</h3><div>The treadmill exercise activates the Nrf2/Keap1 pathway in the hippocampus, thereby reducing CUMS-induced excessive and dysregulated endoplasmic reticulum stress (UPRmt) in an Nrf2-dependent manner, which leads to a recovery of mitochondrial function, suppression of oxidative stress, and improvement of depressive-like behaviors.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"235 ","pages":"Article 111738"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydroxysafflor yellow A protects against ischemic stroke-associated Weber syndrome by inhibiting oxidative stress and alleviating DNA damage","authors":"Miaolin Zeng ,&nbsp;Huifen Zhou ,&nbsp;Lian Zeng ,&nbsp;Man zhang ,&nbsp;Jiehong Yang ,&nbsp;Wujun Geng ,&nbsp;Haitong Wan","doi":"10.1016/j.brainresbull.2026.111747","DOIUrl":"10.1016/j.brainresbull.2026.111747","url":null,"abstract":"<div><div>Weber syndrome, characterized by ipsilateral oculomotor palsy and contralateral hemiplegia, frequently occurs in ischemic stroke cases and is difficult to recover from. Hydroxysafflor yellow A (HSYA), a bioactive component present in <em>Carthamus tinctorius</em> L. and the standardized preparation Danhong injection, has shown protective effects in animal models of various neurological diseases. This research was conducted to evaluate the therapeutic potential of HSYA in ischemic stroke-associated Weber syndrome, while elucidating its mechanistic basis. A rat MCAO model was induced to detect the effects of HSYA on motor dysfunction, ipsilateral ptosis and neuronal death in the right cerebral peduncle. By western blot, immunohistochemistry staining and immunofluorescence staining, we explored the involvement of oxidative stress and DNA damage in HSYA's neuroprotective action. HSYA treatment for consecutive 7 days significantly improved neurological function, grip strength, and asymmetry of bilateral eye clefts in CI/R-injured rats. HSYA also reduced cerebral infarction, preserved neuronal survival, and mitigated histopathological damage in the cerebral peduncle. Mechanistically, HSYA alleviated oxidative stress by preserving CAT, GSH, and SODM levels while inhibiting iNOS overexpression. Furthermore, CI/R injury triggered substantial DNA damage in the cerebral peduncle, as indicated by upregulated levels of 53BP1 and γ-H2A.X. Contents of PARP1, AIF, and MIF were also significantly elevated, accompanied by obvious upregulation of apoptotic cell death, while HSYA treatment effectively attenuated these deleterious effects. HSYA protects against CI/R injury and associated Weber syndrome, and the mechanism involves suppressing oxidative stress and limiting DNA injury.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"235 ","pages":"Article 111747"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting IGF2BP2 alleviates high fat diet aggravated Alzheimer’s disease by inhibiting ferroptosis","authors":"Duobin Zhang ,&nbsp;Lingyun Shao ,&nbsp;Min He ,&nbsp;Shen Yang ,&nbsp;Zhongwu Sun","doi":"10.1016/j.brainresbull.2026.111749","DOIUrl":"10.1016/j.brainresbull.2026.111749","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder whose development is increasingly recognized to be influenced by metabolic factors such as high-fat diet (HFD). HFD can accelerate cognitive decline and exacerbate AD pathology by promoting oxidative stress, neuroinflammation, and lipid dysregulation. Meanwhile, ferroptosis—an iron-dependent form of regulated cell death—has emerged as a key mechanism contributing to neuronal damage in AD. However, the upstream regulators that link HFD-induced stress to ferroptosis and AD progression remain unclear. IGF2BP2, an m⁶A RNA-binding protein, has been implicated in both metabolic regulation and mRNA stability, but its role in AD under HFD conditions has not been fully elucidated.</div></div><div><h3>Methods</h3><div>We established AD models both in vivo and in vitro and subjected them to HFD exposure. Behavioral and biochemical assessments—including Morris water maze, H&amp;E staining, serum triglyceride (TG) and total cholesterol (TC) levels, and ELISA for Aβ and m6A—were conducted. Transcriptomic sequencing identified IGF2BP2 as a differentially expressed gene associated with AD progression under HFD. IGF2BP2 expression was silenced using siRNA in cells and adeno-associated virus (AAV) in rats. Apoptosis, Aβ, TNF-α, IL-1β, and m6A levels were evaluated post-knockdown. Ferroptosis markers (ROS, SOD, GSH, MDA, and SLC7A11) and mitochondrial ultrastructure were also assessed.</div></div><div><h3>Results</h3><div>HFD exacerbated cognitive dysfunction, neuronal damage, lipid metabolism disorder, Aβ accumulation, and m6A hypomodification in AD models. IGF2BP2 expression was significantly elevated in HFD-induced AD, and its knockdown alleviated neuroinflammation, apoptosis, and restored m6A modification. Notably, silencing IGF2BP2 enhanced SLC7A11 expression and reduced ferroptosis-related oxidative stress, mimicking the effects of the ferroptosis inhibitor Fer-1. Moreover, IGF2BP2 knockdown lowered serum TG and TC levels and improved cognitive performance in the Morris water maze.</div></div><div><h3>Conclusion</h3><div>Our findings identify IGF2BP2 as a key mediator linking HFD-induced metabolic dysfunction to AD progression via m6A modification and ferroptosis. Targeting IGF2BP2 may represent a promising therapeutic strategy for AD patients with metabolic comorbidities.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"235 ","pages":"Article 111749"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"miR-669f-5p targeting Dctd contributes to sevoflurane-induced cognitive impairments in aged mice via TLR2/4-MyD88-NF κB pathway\" [Brain Res. Bull. 228 (2025) 111381].","authors":"Yuanping Zhong, Chao Zhang, Yuan Li, Dongqin Chen, Chunchun Tang, Xue Zheng, Zhaoqiong Zhu","doi":"10.1016/j.brainresbull.2025.111695","DOIUrl":"10.1016/j.brainresbull.2025.111695","url":null,"abstract":"","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"111695"},"PeriodicalIF":3.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA Dleu2 regulates fear extinction memory through Celf2-driven synaptic plasticity","authors":"Ziwei Pi ,&nbsp;Jiazhi Jiang ,&nbsp;Lixin Dong ,&nbsp;Ziyue Xu ,&nbsp;Yi Zhang ,&nbsp;Gaomeng Luo ,&nbsp;Junhui Liu ,&nbsp;Runming Liu ,&nbsp;Zhehao Li ,&nbsp;Sha Liu ,&nbsp;Jincao Chen ,&nbsp;Wei Wei ,&nbsp;Xiang Li","doi":"10.1016/j.brainresbull.2026.111757","DOIUrl":"10.1016/j.brainresbull.2026.111757","url":null,"abstract":"<div><div>Long noncoding RNAs (lncRNAs) are diverse regulators that shape many aspects of brain function. Nonetheless, their role in the mechanisms underlying fear extinction memory remains insufficiently explored. We profiled lncRNAs following the RNA capture-seq in the infralimbic prefrontal cortex (ILPFC) and identified the processed-transcript lncRNA deleted in lymphocytic leukemia-2 (Dleu2). The knockdown of Dleu2 by antisense oligonucleotide (ASO) impaired extinction memory, which demonstrated an essential role of Dleu2 in this process. To elucidate the underlying mechanism, CHIRP-seq and ATAC-seq analyses demonstrated an increased binding of Dleu2 within the intronic region of <em>Celf2</em>, accompanied by enhanced chromatin accessibility. This modulation subsequently promotes the transcription of <em>Celf2</em>, a critical gene involved in synaptic plasticity. Functionally, <em>Celf2</em> knockdown in ILPFC recapitulated the fear extinction memory deficit and reduced the number of dendritic spines. Together, these results indicate that lncRNA Dleu2 may serve as a potential therapeutic entry point for memory-related disorders.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111757"},"PeriodicalIF":3.7,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146096062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}