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What Information do Systemic Pathological Changes Bring to the Diagnosis and Treatment of Alzheimer's Disease? 全身病理变化对阿尔茨海默病的诊断和治疗有哪些启示?
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-07-01 Epub Date: 2025-04-21 DOI: 10.1007/s12264-025-01399-z
Jinyue Zhou, Xiaoli Sun, Keren Wang, Min Shen, Jingbo Yu, Qi Yao, Hang Hong, Chunlan Tang, Qinwen Wang
{"title":"What Information do Systemic Pathological Changes Bring to the Diagnosis and Treatment of Alzheimer's Disease?","authors":"Jinyue Zhou, Xiaoli Sun, Keren Wang, Min Shen, Jingbo Yu, Qi Yao, Hang Hong, Chunlan Tang, Qinwen Wang","doi":"10.1007/s12264-025-01399-z","DOIUrl":"10.1007/s12264-025-01399-z","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is regarded as a neurodegenerative disease, and it has been proposed that AD may be a systemic disease. Studies have reported associations between non-neurological diseases and AD. The correlations between AD pathology and systemic (non-neurological) pathological changes are intricate, and the mechanisms underlying these correlations and their causality are unclear. In this article, we review the association between AD and disorders of other systems. In addition, we summarize the possible mechanisms associated with AD and disorders of other systems, mainly from the perspective of AD pathology. Regarding the relationship between AD and systemic pathological changes, we aim to provide a new outlook on the early warning signs and treatment of AD, such as establishing a diagnostic and screening system based on more accessible peripheral samples.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1289-1301"},"PeriodicalIF":5.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031836","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}
引用次数: 0
Multimodal Magnetic Resonance Imaging with Mild Repetitive Head Injury in Awake Rats: Modeling the Human Experience and Clinical Condition. 清醒大鼠轻度重复性头部损伤的多模态磁共振成像:模拟人的经验和临床状况。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-29 DOI: 10.1007/s12264-025-01438-9
Nicole Bens, Arnold Chang, Richard Ortiz, Joshua Leaston, Praveen Kulkarni, Rosemarie Hightower, Sophia Prom, Nicholas O'Hare, Eno Ebong, Craig F Ferris
{"title":"Multimodal Magnetic Resonance Imaging with Mild Repetitive Head Injury in Awake Rats: Modeling the Human Experience and Clinical Condition.","authors":"Nicole Bens, Arnold Chang, Richard Ortiz, Joshua Leaston, Praveen Kulkarni, Rosemarie Hightower, Sophia Prom, Nicholas O'Hare, Eno Ebong, Craig F Ferris","doi":"10.1007/s12264-025-01438-9","DOIUrl":"https://doi.org/10.1007/s12264-025-01438-9","url":null,"abstract":"<p><p>Mild repetitive head injury is a serious health problem with long-term negative consequences. Changes in brain neurobiology were assessed with MRI in a model of head injury designed to reflect the human experience. Rats were maintained on a reverse light-dark cycle and head impacted daily at 24 h intervals over three days while fully awake under red light illumination. There was no neuroradiological evidence of brain damage. Rats were imaged for changes in blood brain barrier permeability, edema and gray matter microarchitecture, and resting state functional connectivity. Data were registered to a 3D MRI rat atlas with 173 segmented brain areas providing site-specific information on each imaging modality. Changes in BBB permeability were minimal and localized to the hippocampus and cerebellum. There was evidence of cytotoxic edema in the basal ganglia, thalamus, and cerebellum. There was a global decrease in connectivity and an increase in gliosis in the thalamus, cerebellum, and hippocampus. This study shows a sequelae of neuropathology caused by mild repetitive head injury that is commonly observed in clinical practice using MRI in patients. As such, it may serve as a model for testing the efficacy of new therapeutics using any or all of the measures as biomarkers to assess drug efficacy.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529070","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}
引用次数: 0
Targeting Phospholipid Metabolism as an Effective Hearing Protection Strategy. 靶向磷脂代谢是有效的听力保护策略。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-28 DOI: 10.1007/s12264-025-01433-0
Huanyu Mao, Wenli Ni, Lupeng Ma, Xiang Li, Yanping Zhang, Yuzheng Zhao, Wenyan Li, Huawei Li, Yan Chen
{"title":"Targeting Phospholipid Metabolism as an Effective Hearing Protection Strategy.","authors":"Huanyu Mao, Wenli Ni, Lupeng Ma, Xiang Li, Yanping Zhang, Yuzheng Zhao, Wenyan Li, Huawei Li, Yan Chen","doi":"10.1007/s12264-025-01433-0","DOIUrl":"https://doi.org/10.1007/s12264-025-01433-0","url":null,"abstract":"<p><p>Cochlear hair cell (HC) damage is a primary cause of sensorineural hearing loss. In this study, we performed metabolomic profiling of cochlear sensory epithelium following neomycin-induced HC injury and identified elevated arginine metabolism as a key metabolic characteristic of damaged HCs. Using a highly sensitive and specific biosensor, we confirmed that injury induced an increase in arginine levels within cochlear HCs. By manipulating the levels of arginine and its downstream metabolites, we discovered that unmetabolized arginine exerts a strong protective effect on cochlear HCs, independent of its downstream metabolites, such as nitric oxide. Furthermore, integrated metabolomic and transcriptomic analyses revealed that arginine plays a critical role in reprogramming phospholipid metabolism. Arginine supplementation enhanced membrane phospholipid saturation through the Lands cycle and de novo lipogenesis, and protected HCs from phospholipid peroxidation-induced membrane damage and subsequent cell death. Notably, arginine supplementation protected hearing from both noise- and aminoglycoside-induced injury in mice. These findings underscore the role of unmetabolized arginine in modulating phospholipid metabolism and preventing membrane damage in cochlear HCs, highlighting that targeting phospholipid metabolism is an effective hearing protection strategy.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529071","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}
引用次数: 0
Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model. APP/PS1小鼠模型中白内障加重阿尔茨海默样病理和认知缺陷
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-28 DOI: 10.1007/s12264-025-01442-z
Zhao Geng, Zhong-Yuan Yu, Jun Tan, Xuan-Yue Wang, Gui-Hua Zeng, Jiang-Hui Li, Yu-Di Bai, Xiao-Qin Zeng, Yu-Peng Zhu, Cheng-Rong Tan, An-Yu Shi, Yu-Hui Liu, Xian-Le Bu, Zi Ye, Yan-Jiang Wang, Zhao-Hui Li
{"title":"Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model.","authors":"Zhao Geng, Zhong-Yuan Yu, Jun Tan, Xuan-Yue Wang, Gui-Hua Zeng, Jiang-Hui Li, Yu-Di Bai, Xiao-Qin Zeng, Yu-Peng Zhu, Cheng-Rong Tan, An-Yu Shi, Yu-Hui Liu, Xian-Le Bu, Zi Ye, Yan-Jiang Wang, Zhao-Hui Li","doi":"10.1007/s12264-025-01442-z","DOIUrl":"https://doi.org/10.1007/s12264-025-01442-z","url":null,"abstract":"<p><p>Clinical investigations have suggested a potential link between cataracts and Alzheimer's disease (AD). However, whether cataract has an impact on the progression of AD remains unclear. The objective of this research was to determine the relationship between cataracts and AD. A cataract model was established in APP/PS1 [mutant amyloid precursor protein (APP) and a mutant presenilin-1 (PS1) gene] mice via lens puncture. Behavioural assays were used to evaluate cognitive function. Immunohistochemistry, immunofluorescence, and enzyme-linked immunosorbent assays (ELISA) were applied to detect AD-related pathology. Visual signals were markedly obstructed following surgery to induce cataracts, and these mice presented an increased cerebral amyloid-beta (Aβ) load, while no significant alterations in the levels of enzymes associated with Aβ metabolism were detected. In addition, compared with control mice, cataract model mice presented increased astrogliosis and microgliosis, along with elevated levels of proinflammatory factors. Moreover, cataract model mice presented more pronounced cognitive impairments than did control mice. Our study offers experimental confirmation that cataract considerably contributes to the pathogenesis of AD, thereby emphasizing the importance of visual signals in maintaining cognitive well-being.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529069","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}
引用次数: 0
Bridging the Gap: The Neuro-immune Axis as a Key Player in Neurodegenerative Disorders. 弥合差距:神经免疫轴在神经退行性疾病中的关键作用。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-25 DOI: 10.1007/s12264-025-01439-8
Tingting Liu, Haojie Wu, Jianshe Wei
{"title":"Bridging the Gap: The Neuro-immune Axis as a Key Player in Neurodegenerative Disorders.","authors":"Tingting Liu, Haojie Wu, Jianshe Wei","doi":"10.1007/s12264-025-01439-8","DOIUrl":"https://doi.org/10.1007/s12264-025-01439-8","url":null,"abstract":"<p><p>Neurodegenerative diseases encompass a diverse array of disorders that have a profoundly detrimental impact on human health, characterized by their intricate and multifaceted pathogenesis. In the recent past, a growing body of scientific research has begun to shed light on the critical involvement of the neuro-immune axis in the onset and advancement of these debilitating conditions. This comprehensive review article delves into the intricate composition of the neuro-immune axis, elucidating the complex mechanisms through which it exerts its influence in the context of neurodegenerative diseases. Furthermore, it explores the potential therapeutic applications of targeting the neuro-immune axis for the management and treatment of these diseases. This extensive examination aims to offer new perspectives and innovative strategies that could pave the way for more effective treatments for neurodegenerative diseases, thereby providing hope for those afflicted by these challenging conditions.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144485210","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}
引用次数: 0
Csde1 Mediates Neurogenesis via Post-transcriptional Regulation of the Cell Cycle. Csde1通过细胞周期转录后调控介导神经发生。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-24 DOI: 10.1007/s12264-025-01426-z
Xiangbin Jia, Wenqi Xie, Bing Du, Mei He, Jia Chen, Meilin Chen, Ge Zhang, Ke Wang, Wanjing Xu, Yuxin Liao, Senwei Tan, Yongqing Lyu, Bin Yu, Zihang Zheng, Xiaoyue Sun, Yang Liao, Zhengmao Hu, Ling Yuan, Jieqiong Tan, Kun Xia, Hui Guo
{"title":"Csde1 Mediates Neurogenesis via Post-transcriptional Regulation of the Cell Cycle.","authors":"Xiangbin Jia, Wenqi Xie, Bing Du, Mei He, Jia Chen, Meilin Chen, Ge Zhang, Ke Wang, Wanjing Xu, Yuxin Liao, Senwei Tan, Yongqing Lyu, Bin Yu, Zihang Zheng, Xiaoyue Sun, Yang Liao, Zhengmao Hu, Ling Yuan, Jieqiong Tan, Kun Xia, Hui Guo","doi":"10.1007/s12264-025-01426-z","DOIUrl":"https://doi.org/10.1007/s12264-025-01426-z","url":null,"abstract":"<p><p>Loss-of-function variants in CSDE1 have been strongly linked to neuropsychiatric disorders, yet the precise role of CSDE1 in neurogenesis remains elusive. In this study, we demonstrate that knockout of Csde1 during cortical development in mice results in impaired neural progenitor proliferation, leading to abnormal cortical lamination and embryonic lethality. Transcriptomic analysis revealed that Csde1 upregulates the transcription of genes involved in the cell cycle network. Applying a dual thymidine-labelling approach, we further revealed prolonged cell cycle durations of neuronal progenitors in Csde1-knockout mice, with a notable extension of the G1 phase. Intersection with CLIP-seq data demonstrated that Csde1 binds to the 3' untranslated region (UTR) of mRNA transcripts encoding cell cycle genes. Particularly, we uncovered that Csde1 directly binds to the 3' UTR of mRNA transcripts encoding Cdk6, a pivotal gene in regulating the transition from the G1 to S phases of the cell cycle, thereby maintaining its stability. Collectively, this study elucidates Csde1 as a novel regulator of Cdk6, sheds new light on its critical roles in orchestrating brain development, and underscores how mutations in Csde1 may contribute to the pathogenesis of neuropsychiatric disorders.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144485211","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}
引用次数: 0
From Correlation to Causation: Understanding Episodic Memory Networks. 从相关性到因果关系:理解情景记忆网络。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-24 DOI: 10.1007/s12264-025-01407-2
Ahsan Khan, Jing Liu, Maité Crespo-García, Kai Yuan, Cheng-Peng Hu, Ziyin Ren, Chun-Hang Eden Ti, Desmond J Oathes, Raymond Kai-Yu Tong
{"title":"From Correlation to Causation: Understanding Episodic Memory Networks.","authors":"Ahsan Khan, Jing Liu, Maité Crespo-García, Kai Yuan, Cheng-Peng Hu, Ziyin Ren, Chun-Hang Eden Ti, Desmond J Oathes, Raymond Kai-Yu Tong","doi":"10.1007/s12264-025-01407-2","DOIUrl":"https://doi.org/10.1007/s12264-025-01407-2","url":null,"abstract":"<p><p>Episodic memory, our ability to recall past experiences, is supported by structures in the medial temporal lobe (MTL) particularly the hippocampus, and its interactions with fronto-parietal brain regions. Understanding how these brain regions coordinate to encode, consolidate, and retrieve episodic memories remains a fundamental question in cognitive neuroscience. Non-invasive brain stimulation (NIBS) methods, especially transcranial magnetic stimulation (TMS), have advanced episodic memory research beyond traditional lesion studies and neuroimaging by enabling causal investigations through targeted magnetic stimulation to specific brain regions. This review begins by delineating the evolving understanding of episodic memory from both psychological and neurobiological perspectives and discusses the brain networks supporting episodic memory processes. Then, we review studies that employed TMS to modulate episodic memory, with the aim of identifying potential cortical regions that could be used as stimulation sites to modulate episodic memory networks. We conclude with the implications and prospects of using NIBS to understand episodic memory mechanisms.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144485212","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}
引用次数: 0
Recent Advances in the Molecular Mechanisms of Ocular Dominance Plasticity in the Visual Cortex. 视觉皮层眼优势可塑性分子机制的研究进展。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-24 DOI: 10.1007/s12264-025-01448-7
Yanglin Qin, Wei Wang, Yu Gu, Xuefeng Shi
{"title":"Recent Advances in the Molecular Mechanisms of Ocular Dominance Plasticity in the Visual Cortex.","authors":"Yanglin Qin, Wei Wang, Yu Gu, Xuefeng Shi","doi":"10.1007/s12264-025-01448-7","DOIUrl":"https://doi.org/10.1007/s12264-025-01448-7","url":null,"abstract":"<p><p>The visual cortex is an essential part of the brain for processing visual information. It exhibits structural and functional plasticity, which is crucial for adapting to complex visual environments. The quintessential manifestation of visual cortical plasticity is ocular dominance plasticity during the critical period, which involves numerous cellular and molecular events. While previous studies have emphasized the role of visual cortical neurons and their associated functional molecules in visual plasticity, recent findings have revealed that structural factors such as the extracellular matrix and glia are also involved. Investigating how these molecules interact to form a complex network that facilitates plasticity in the visual cortex is crucial to our understanding of the development of the visual system and the advancement of therapeutic strategies for visual disorders like amblyopia.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476144","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}
引用次数: 0
From Brain to Shopping Cart: Neural Signals of Willingness to Buy Innovative Products. 从大脑到购物车:购买创新产品意愿的神经信号。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-24 DOI: 10.1007/s12264-025-01431-2
Ziyi Li, Lulu Liu, Ying Hu, Lushuang Zhang, Xingxu Xie, Jing Luo
{"title":"From Brain to Shopping Cart: Neural Signals of Willingness to Buy Innovative Products.","authors":"Ziyi Li, Lulu Liu, Ying Hu, Lushuang Zhang, Xingxu Xie, Jing Luo","doi":"10.1007/s12264-025-01431-2","DOIUrl":"https://doi.org/10.1007/s12264-025-01431-2","url":null,"abstract":"<p><p>Exploring the mechanisms underlying willingness to buy (WTB) will help us identify neural indicators for predicting the performance of innovative products. Using functional magnetic resonance imaging, we asked participants to view products created by combining two components, including high applicability new combinations (HANCs), which provide a novel and practical application; and low applicability new combinations (LANCs), which provide no additional value. First, we found that WTB generally involves activation of the parahippocampal gyrus. For HANC, activation in the pars opercularis of the inferior frontal gyrus (IFG oper) is associated with WTB. Second, representational similarity analysis revealed that for HANC, the interrelation between the elements and combinations in the IFG oper predicts WTB. Third, multivoxel pattern analysis found that classification accuracy in the IFG oper predicts the difference in WTB between HANCs and LANCs. In conclusion, WTB requires default mode network-based associative processing. For HANC products, executive control network-based processes are necessary for value construction.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476143","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}
引用次数: 0
Enhanced Therapeutic Effects of Extracellular Vesicles Targeting MiR-137 Contribute to Functional Recovery by Attenuating Neuronal Injury After Ischemic Stroke. 靶向MiR-137的细胞外囊泡增强的治疗效果通过减轻缺血性卒中后神经元损伤有助于功能恢复。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-06-23 DOI: 10.1007/s12264-025-01437-w
Hui-Xin Zhang, Li-Qing Tao, Yi-Hang Chen, Tian-Yi Jiang, Zhi-Yuan Ye, Wen She, Chang-Ying Chen, Ya-Li Han, Cui Qi, Chong Shen, Jun Gao
{"title":"Enhanced Therapeutic Effects of Extracellular Vesicles Targeting MiR-137 Contribute to Functional Recovery by Attenuating Neuronal Injury After Ischemic Stroke.","authors":"Hui-Xin Zhang, Li-Qing Tao, Yi-Hang Chen, Tian-Yi Jiang, Zhi-Yuan Ye, Wen She, Chang-Ying Chen, Ya-Li Han, Cui Qi, Chong Shen, Jun Gao","doi":"10.1007/s12264-025-01437-w","DOIUrl":"https://doi.org/10.1007/s12264-025-01437-w","url":null,"abstract":"<p><p>Ischemic stroke is a leading cause of death, especially among aging populations. MicroRNA-137 (miR-137) is known to be involved in neurodevelopment. However, its role in ischemic stroke is still unexplored. Here, we assessed the regulation of miR-137 after cerebral ischemia and reperfusion (I/R) and developed a targeted delivery therapy by extracellular vesicles (EVs). Our results showed that miR-137 was enhanced in the hippocampus of mice after I/R. miR-137 regulated the ischemia-induced cell death by decreasing the expression of Sirtuin1 (Sirt1). Therefore, we evaluated a therapeutic approach involving mesenchymal stem cell-derived EVs. Systemic delivery of anti-miR-137 by rabies virus glycoprotein-modified EVs allowed specific targeting of neurons. After anti-miR-137 treatment, the survival rate was increased in ischemic mice, and some neurobehavioral deficits were alleviated. We also established that Maged1 deficiency attenuated ischemic damage and inhibited miR-137 enrichment. Besides, the increase of miR-137 increased neuronal death and neurological deficits after I/R through the MAGED1/miR-137/Sirt1 pathway. Combined with rabies virus glycoprotein-modified EVs and anti-miR-137, this is a new strategy for regulating ischemic neuronal injury and functional recovery by targeting miR-137.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476142","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}
引用次数: 0
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