Experimental Neurobiology最新文献

Application of Neurotrophic Factors as a Therapeutic Approach for Neurodegenerative Diseases. 神经营养因子在神经退行性疾病治疗中的应用。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-10-01 DOI: 10.5607/en25023

Seung Chan Kim, Shin Young Lee, Un Ju Jung, Sang Ryong Kim

引用次数: 0

The Pre-clincal Safety of Graphene-based Electrodes Implanted on Rat Cerebral Cortex. 石墨烯电极植入大鼠大脑皮层的临床前安全性研究。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-09-23 DOI: 10.5607/en25018

Gaeun Kim, Hyerin Jeong, Kyungtae Kim, Sangwon Lee, Eunha Baeg, Sungchil Yang, Byoungkwan Kim, Sunggu Yang

{"title":"The Pre-clincal Safety of Graphene-based Electrodes Implanted on Rat Cerebral Cortex.","authors":"Gaeun Kim, Hyerin Jeong, Kyungtae Kim, Sangwon Lee, Eunha Baeg, Sungchil Yang, Byoungkwan Kim, Sunggu Yang","doi":"10.5607/en25018","DOIUrl":"https://doi.org/10.5607/en25018","url":null,"abstract":"Graphene has emerged as a promising nanomaterial for brain-computer interface (BCI) applications due to its excellent electrical properties and biocompatibility. However, its long-term structural compatibility on the cerebral cortex requires further validation. This study assessed both functional compatibility and preservation of neural tissue architecture for graphene/parylene C composite electrodes implanted on the rat cortical surface, in accordance with ISO 10993-6 guideline weekly neurobehavioral assessments and comprehensive histopathological analyses were conducted for four weeks post-implantation. Our results revealed no significant differences in neurobehavioral outcomes between graphene-based and medical-grade silicone implants. Histopathological examination showed no noticeable inflammatory responses, changes in cellular morphology, myelination status, or neuronal degeneration. These findings indicate that graphene electrodes preserve tissue integrity comparable to medical‑grade silicone. Our study supports graphene's potential use in clinical neuroprosthetics and neuromodulation devices.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124634","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}

引用次数: 0

KCC-07, MBD2 Inhibitor, Expands the Therapeutic Window of DNA Damage Inducing Reagents in Neural Tumor Cells. MBD2抑制剂KCC-07扩大DNA损伤诱导试剂对神经肿瘤细胞的治疗窗口

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-08-31 DOI: 10.5607/en25017

Darom Lee, Junyoung Kim, Keeeun Kim, Youngsoo Lee

{"title":"KCC-07, MBD2 Inhibitor, Expands the Therapeutic Window of DNA Damage Inducing Reagents in Neural Tumor Cells.","authors":"Darom Lee, Junyoung Kim, Keeeun Kim, Youngsoo Lee","doi":"10.5607/en25017","DOIUrl":"10.5607/en25017","url":null,"abstract":"Neural tumors represent diverse malignancies with distinct molecular profiles and present particular challenges due to the blood-brain barrier, heterogeneous molecular etiology including epigenetic dysregulation, and the affected organ's critical nature. KCC-07, a selective and blood-brain barrier penetrable MBD2 (methyl CpG binding domain protein 2) inhibitor, can suppress tumor development by inducing p53 signaling, proven only in medulloblastoma. Here we demonstrate KCC-07 treatment's application to other neural tumors. KCC-07 treatment reduced proliferation rates of U-87MG (glioma cell line) and SH-SY5Y (neuroblastoma cell line). p53 stabilization occurred in these cell lines without significantly affecting programmed cell death factors under KCC-07 exposure. Furthermore, tumor cell growth inhibition was enhanced when combined with DNA damaging reagents. Both phleomycin (radiomimetic agent inducing DNA double strand breaks) and etoposide (topoisomerase II inhibitor inducing DNA double strand breaks) treatment activated p53-dependent signaling for apoptosis and cell cycle arrest, consequently suppressing tumor cell growth. Dual treatment with KCC-07 (epigenetic modifier) and DNA damaging reagents augmented tumor cell suppression, suggesting greater benefits of combinatorial therapy for neural tumors than previously demonstrated.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 4","pages":"138-146"},"PeriodicalIF":2.1,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029256","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}

引用次数: 0

Elevated O-GlcNAcylation Enhances Metabolic Rate and Reduces the Excitability of Hypothalamic ARC Neurons in 10-month-old Male Mice. 升高的o - glcn酰化可提高10月龄雄性小鼠下丘脑ARC神经元的代谢率并降低其兴奋性。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-08-31 DOI: 10.5607/en25012

Tamanna Yasmin, Yuna Lee, Hongik Hwang, Jiyeon Seo, Min Soo Kim, Mikyoung Park, Soo-Jin Oh, Min-Ho Nam, Hyewhon Rhim

{"title":"Elevated O-GlcNAcylation Enhances Metabolic Rate and Reduces the Excitability of Hypothalamic ARC Neurons in 10-month-old Male Mice.","authors":"Tamanna Yasmin, Yuna Lee, Hongik Hwang, Jiyeon Seo, Min Soo Kim, Mikyoung Park, Soo-Jin Oh, Min-Ho Nam, Hyewhon Rhim","doi":"10.5607/en25012","DOIUrl":"10.5607/en25012","url":null,"abstract":"Aging correlates with alterations in metabolism and neuronal function, which affect the overall regulation of energy homeostasis. Recent studies have highlighted that protein O-GlcNAcylation, a common post-translational modification regulating metabolic function, is linked to aging. In particular, elevated O-GlcNAcylation increases energy expenditure, potentially due to alterations in the neuronal function of the hypothalamic arcuate nucleus (ARC), a key brain region for energy balance and metabolic processes. However, its impact on metabolism and hypothalamic neuronal activity in aged mice remains unknown. This study investigates the effect of elevated O-GlcNAcylation on metabolic rate, motor behaviors, glucose tolerance, and neuronal excitability within the hypothalamic ARC in 10-month-old mice. We demonstrate that Oga+/- mice with elevated O-GlcNAcylation levels show increased energy expenditure, but do not show significant alterations in motor function or glucose tolerance. Our ex vivo electrophysiology experiments revealed that Oga+/- mice exhibited a reduced firing rate of hypothalamic ARC neurons, suggesting that the increased metabolism in these mice could be attributed to the reduced activity of ARC neurons. These findings indicate that O-GlcNAcylation plays a crucial role in maintaining metabolic balance and neuronal function in the aging brain.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 4","pages":"147-155"},"PeriodicalIF":2.1,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029279","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}

引用次数: 0

Reproductive Dysfunction in Experimental Autoimmune Encephalomyelitis, an Animal Model of Multiple Sclerosis. 多发性硬化症动物模型——实验性自身免疫性脑脊髓炎的生殖功能障碍

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-08-31 DOI: 10.5607/en25021

Taekyun Shin, Seung Joon Kim, Taeyoung Kang, Hyohoon Jeong, Meejung Ahn, Kyungsook Jung, Jeongtae Kim

{"title":"Reproductive Dysfunction in Experimental Autoimmune Encephalomyelitis, an Animal Model of Multiple Sclerosis.","authors":"Taekyun Shin, Seung Joon Kim, Taeyoung Kang, Hyohoon Jeong, Meejung Ahn, Kyungsook Jung, Jeongtae Kim","doi":"10.5607/en25021","DOIUrl":"10.5607/en25021","url":null,"abstract":"Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS). The latter is a human organ-specific autoimmune disease of the central nervous system (CNS). EAE is characterized by systemic inflammation associated with increased blood levels of proinflammatory mediators that potentially trigger inflammation of both reproductive organs and the CNS. Pathological changes in the hypothalamus-pituitary gland-gonadal axis have occasionally been reported in both the MS and EAE contexts. Such changes may affect the reproductive organs. We used the phrase \"EAE and hypothalamus-pituitary-gonads (testis and ovary)\" to retrieve relevant papers from PubMed. We postulated that EAE might be associated with inflammation of the hypothalamus, pituitary gland and gonads, in turn indicating reproductive dysfunction. This paper overviews evidence supporting the roles of both hormonal and inflammatory alterations in animals with EAE. This aids our understanding of how certain autoimmune diseases are associated with infertility.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 4","pages":"131-137"},"PeriodicalIF":2.1,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029298","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}

引用次数: 0

Differences in Learning Strategy Selection and Object Location Memory Impairments in APP/PS1 Mice. APP/PS1小鼠学习策略选择与目标定位记忆障碍的差异

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-08-31 DOI: 10.5607/en25013

Yoon-Sun Jang, Dong-Hee Kim, Won Kyung Jeon, Jung-Soo Han

{"title":"Differences in Learning Strategy Selection and Object Location Memory Impairments in APP/PS1 Mice.","authors":"Yoon-Sun Jang, Dong-Hee Kim, Won Kyung Jeon, Jung-Soo Han","doi":"10.5607/en25013","DOIUrl":"10.5607/en25013","url":null,"abstract":"This study investigated the learning strategy preferences of 11-month-old APP/PS1 double transgenic (Tg) mice, a well-established murine model of Alzheimer's disease (AD). APP/PS1 Tg and non-Tg control mice were serially trained in visual and hidden platform tasks in the Morris water maze. APP/PS1 Tg mice performed poorly in visual platform training compared with non-Tg mice but performed as well as non-Tg mice in hidden platform training. Further analysis of their search paths for locating a hidden platform revealed that APP/PS1 Tg mice used more cued/response search patterns than place/spatial search patterns compared with non-Tg mice. Three months later, the object/location recognition memory of APP/PS1 Tg mice was assessed. Although their object recognition memory was intact, their object location memory was impaired. Neuropathological AD features of APP/PS1 transgenic mice were observed in the medial prefrontal cortex, retrosplenial cortex, and hippocampus, key brain regions involved in learning strategy shifts and spatial cognition. These results indicate that distinct search patterns and spatial memory deficits in APP/PS1 Tg mice are key features of AD animal models.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 4","pages":"156-167"},"PeriodicalIF":2.1,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12426418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029112","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}

引用次数: 0

The Role of Agmatine in Modulating Autophagy Under Neuroinflammatory Conditions Induced by Metabolic Alteration in Mouse Brain. 胍丁氨酸在小鼠脑代谢改变诱导的神经炎症条件下调节自噬的作用。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 DOI: 10.5607/en25007

Ji Young Chang, Jiwon Kim, Renée Kosonen, Jong Youl Kim, Jong Eun Lee

{"title":"The Role of Agmatine in Modulating Autophagy Under Neuroinflammatory Conditions Induced by Metabolic Alteration in Mouse Brain.","authors":"Ji Young Chang, Jiwon Kim, Renée Kosonen, Jong Youl Kim, Jong Eun Lee","doi":"10.5607/en25007","DOIUrl":"10.5607/en25007","url":null,"abstract":"Changes in microglia, a specialized population of glial cells found in the central nervous system (CNS), is often associated with hyperglycemic conditions. It has been reported that exogenous administration of agmatine (agm) has neuroprotective effects in CNS injuries, including neurodegenerative diseases, while also being involved with modulating macrophage subdivision. In this study, the effects of agmatine on microglial polarization has been investigated and whether this effect can be related to the modulation of autophagy in neuroinflammatory conditions induced by high glucose (HG) concentrations. Neuroinflammatory conditions were mimicked through treatment to BV2 microglial cells. BV2 cells were mainly induced into proinflammatory M1 phenotype when treated with HG (100 mM), shown by the increase in M1 marker, CD86, and shifted to M2 phenotype in HG condition with agm (100 μM), indicated by the upregulation of mannose receptor CD206. When agm was treated with HG, the level of LC3-II was increased while p62/SQSTM1 level was downregulated, and the expression of LAMP1 was increased. In transmission electron microscopy, autophagosomes has shown that HG conditions led to severe mitochondrial damage while elongating phagophore membranes and autolysosomes were seen in cells treated with HG and agm, showing stimulated mitophagy. In a high-fat diet-induced T2DM metabolic dementia animal model, agmatine administration upregulated autophagy and shifted microglial polarization from proinflammatory to anti-inflammatory phenotype, improving cognitive function and alleviating neuroinflammation. In this study, it has been demonstrated that agm treatment can ameliorate neuroinflammation by upregulating autophagy on a cellular level and shifting microglia polarization from M1 to M2 phenotype, showing a therapeutic potential in metabolic AD.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 3","pages":"95-107"},"PeriodicalIF":2.1,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552794","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}

引用次数: 0

Domain-generalized Deep Learning for Improved Subject-independent Emotion Recognition Based on Electroencephalography. 基于脑电图的改进主题无关情绪识别的领域广义深度学习。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 Epub Date: 2025-05-14 DOI: 10.5607/en25011

Jung-Hwan Kim, Hyerin Nam, Doyeon Won, Chang-Hwan Im

{"title":"Domain-generalized Deep Learning for Improved Subject-independent Emotion Recognition Based on Electroencephalography.","authors":"Jung-Hwan Kim, Hyerin Nam, Doyeon Won, Chang-Hwan Im","doi":"10.5607/en25011","DOIUrl":"10.5607/en25011","url":null,"abstract":"Electroencephalography (EEG) provides high temporal resolution and noninvasiveness for a range of practical applications, including emotion recognition. However, inherent variability across subjects poses significant challenges to model generalizability. In this study, we systematically evaluated twelve approaches by combining four domain generalization (DG) techniques, Deep CORAL, GroupDRO, VREx, and DANN, with three representative deep learning architectures (ShallowFBCSPNet, EEGNet, and TSception) to enable improved subject-independent EEG-based emotion recognition. The performances of the DG-integrated deep learning models were quantitatively evaluated using two emotional EEG datasets collected by the authors. Data from each subject were treated as distinct domains in each model. Binary classification tasks were conducted to identify the valence or arousal state of each participant based on a ten-fold cross-validation strategy. The results indicated that the application of DG methods consistently enhanced classification accuracy across datasets. In one dataset, TSception combined with VREx achieved the highest performance for both valence and arousal classifications. In the other dataset, TSception with VREx still yielded the highest valence classification accuracy, while TSception combined with GroupDRO showed the best arousal classification performance among the twelve models, slightly outperforming TSception with VREx. These findings underscore the potential of DG approaches to mitigate distributional shifts caused by intersubject and intersession variabilities to implement robust subject-independent EEG-based emotion recognition systems.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":"119-130"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971614","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}

引用次数: 0

The Neurotoxic Properties of α-synuclein Polymorphs. α-突触核蛋白多态性的神经毒性。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 DOI: 10.5607/en25016

Katherine Chang, Zulfeqhar Syed, Valentina Baena, Mark R Cookson, Changyoun Kim

{"title":"The Neurotoxic Properties of α-synuclein Polymorphs.","authors":"Katherine Chang, Zulfeqhar Syed, Valentina Baena, Mark R Cookson, Changyoun Kim","doi":"10.5607/en25016","DOIUrl":"10.5607/en25016","url":null,"abstract":"Progressive neurodegeneration is a common pathological feature of synucleinopathies, which include dementia with Lewy bodies (DLB), Parkinson's disease (PD), and multiple system atrophy (MSA). Among mechanisms known to induce neurodegeneration, the presence of aggregated forms of α-synuclein (α-syn) has been extensively considered as a causal factor for cell death. These aggregates exist in multiple different physical forms, which might yield different disease phenotypes and explain the heterogeneity among these diseases. Here, we investigated the neurotoxic properties of structurally distinct and exogenous α-syn polymorphs. Most of the polymorphs at the concentrations we studied are neurotoxic, but dopamine stabilized α-syn oligomer induced greater levels of neurotoxicity at lower concentrations compared to other polymorphs. In addition, polymorphs commonly induced apoptotic neuronal death through autophagic impairment. Our results suggest that neurons have different sensitivities to different α-syn aggregates, which should be a consideration when developing disease markers and therapeutics.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 3","pages":"87-94"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552793","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}

引用次数: 0

Robust Neuroprotection by NEMO (IKKγ)-binding Domain Peptide via Anti-inflammatory Effects in the Post-ischemic Brain. NEMO （IKKγ）结合区域肽通过抗炎作用在缺血后脑中的强大神经保护作用

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 DOI: 10.5607/en25020

Sang-A Oh, Song-I Seol, Ja-Kyeong Lee, Il-Doo Kim

{"title":"Robust Neuroprotection by NEMO (IKKγ)-binding Domain Peptide via Anti-inflammatory Effects in the Post-ischemic Brain.","authors":"Sang-A Oh, Song-I Seol, Ja-Kyeong Lee, Il-Doo Kim","doi":"10.5607/en25020","DOIUrl":"10.5607/en25020","url":null,"abstract":"Microglia exhibit a complex and context-dependent role in the post-ischemic brain, performing both neuroprotective and neurotoxic functions. Among the many factors contributing to pro-inflammatory microglia activation, NF-κB signaling plays a pivotal role. The NEMO (IKKγ)-binding domain (NBD) peptide, an 11-amino-acids cell-permeable peptide spanning the NBD of IKKα and IKKβ, acts as a highly specific inhibitor by preventing NEMO-IKKα/IKKβ complex formation. We investigated the neuroprotective effects of the NBD peptide in a post-ischemic brain using a transient middle cerebral artery occlusion (MCAO) animal model. In in vitro experiments, pre-treatment of BV2 cells (a microglia cell line) with NBD peptide significantly suppressed LPS-induced NEMO-IKKα/IKKβ complex formation, nuclear translocation of p65, and upregulation of numerous pro-inflammatory cytokines expressions. The anti-inflammatory effect was further confirmed in reporter gene assay following reporter plasmid transfection, demonstrating a NBD peptide dose-dependent response. In the post-ischemic brain, intranasal delivery of NBD peptide significantly suppressed NEMO-IKKα/IKKβ complex formation, IκB-α phosphorylation, microglial activation, and cytokine induction. Notably, intranasal administration of NBD peptide 3 h post-MCAO significantly reduced infarct volumes in a dose-dependent manner. A significant reduction in infarct volume was observed by 6 h post-administration, suggesting an extended therapeutic window for the NBD peptide. These neuroprotective effects were accompanied by the attenuation of neurological deficits and motor function impairment, as assessed by rota-rod, beam balance, and corner turn tests. Collectively, these results highlight a robust neuroprotective effect along with long-term outcomes of NBD peptide in the post-ischemic brain, with NBD peptide-mediated blocking of NEMO-IKKα/IKKβ complex formation serving as a key underlying molecular mechanism.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 3","pages":"108-118"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552792","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}

引用次数: 0