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中国神经再生研究（英文版）
中国康复医学会
中国神经再生研究（英文版）

中国康复医学会

旬刊

1673-5374

bwb@nrronline.com

024-23381085

110004

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中国神经再生研究（英文版）/Journal Neural Regeneration ResearchCSCDCSTPCD北大核心SCI
查看更多>>SCI收录杂志！！！ 本刊为英文版杂志，以国际通用语言研究最前沿、最热点的神经再生问题。创刊起点高，评估论文研究成果的学术标准高，对论文语言表述水平的要求高。 刊物宗旨： 2006年创刊，面向国际、立足国际，以办好一本国际神经再生学科界专家公认的专业性学术期刊为工作目标，主要发表神经再生领域基础及应用基础研究方面的学术文章。 出版重点： 2009年本刊重点出版对神经损伤修复过程中原位神经干细胞以及移植的神经干细胞作用机制的研究，出版神经组织工程、神经退行性疾病组织形态学变化以及中医药对神经细胞、神经组织再生过程中生理、病理结构变化影响的相关研究文章。面向国际，立足国际，关注全球范围内具有创新性的抑制、促进或影响神经细胞、神经组织再生结构变化相关机制的研究，关注由此而发生的一系列功能变化及其相互关系。 感兴趣神经解剖学、病理学、生理学、生物化学、药理学、免疫学、发育学等来自多学科、多层面的题材，感兴趣发表以基础实验性研究为主的揭示大脑皮质、海马、松果体、神经胶质细胞、脊髓神经元、周围神经元以及运动和感觉神经损伤与再生的研究原著，对有助于认识神经再生正常和异常机制的临床类文章，如罕见病例报告、调查分析等也可纳入范围。 欢迎文章从理论假设、研究方法、模型制备、影像学技术等多个视角描述神经再生的相关特点，为读者提供该领域最有价值的学科进展信息及其最新的理论观点，增强对神经再生复杂机制、学说和病理发生过程的理解。一般文章2000-4000单词。 非常注重出版时效。投稿15～30天编辑部采用随机盲法抽取国际评审专家审稿，符合采用标准的文章进入修稿程序，力求出版周期120～180天，以保证高质量优秀稿件抢先出版。 收录情况： 科学引文索引（SCI） 2006年被SCI引文库收录8篇 2008年1月至2008年7月被SCI收录文章188篇 美国生物学文献数据库（BIOSIS） 美国《化学文摘》（CA） 荷兰《医学文摘库/医学文摘》（EM） 波兰《哥伯尼索引》（IC） 中国英文版科技期刊数据库(统计源期刊) 中国科学引文数据库（核心期刊） 2007年被CA收录247篇，被EM收录173篇
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    Proteostasis failure:at the intersection between aging and Alzheimer's disease

    Natalia PobleteClaudio Hetz
    3221-3222页
      原文链接:
    • 万方数据

    Targeting Epac2 and GluA3-containing AMPARs:a novel therapeutic strategy for Alzheimer's disease

    Tong ZhangMartina Schmidt
    3223-3224页
      原文链接:
    • 万方数据

    Context-dependency in medicine:how neuronal excitability influences the impact of dopamine on cognition

    Mahboubeh AhmadiNahid RouhiJavad Mirnajafi-ZadehBechara J.Saab...
    3225-3226页
      原文链接:
    • 万方数据
    • 维普

    Role of resident memory T cells in neuroinflammatory and neurodegenerative diseases in the central nervous system

    Kimitoshi Kimura
    3227-3228页
      原文链接:
    • 万方数据
    • 维普

    Biochemical dissection of STAT3 signaling in amyotrophic lateral sclerosis

    Savina ApolloniNadia D'Ambrosi
    3229-3230页
      原文链接:
    • 万方数据
    • 维普

    Secretome of polarized macrophages:potential for targeting inflammatory dynamics in spinal cord injury

    Andreia MonteiroSusana MonteiroNuno A.Silva
    3231-3232页
      原文链接:
    • 万方数据
    • 维普

    The Citron homology domain of MAP4Ks improves outcomes of traumatic brain injury

    Xiaoling ZhongWenjiao TaiMeng-Lu LiuShuaipeng Ma...
    3233-3244页
    查看更多>>摘要：The mitogen-activated protein kinase kinase kinase kinases(MAP4Ks)signaling pathway plays a pivotal role in axonal regrowth and neuronal degeneration following insults.Whether targeting this pathway is beneficial to brain injury remains unclear.In this study,we showed that adeno-associated virus-delivery of the Citron homology domain of MAP4Ks effectively reduces traumatic brain injury-induced reactive gliosis,tauopathy,lesion size,and behavioral deficits.Pharmacological inhibition of MAP4Ks replicated the ameliorative effects observed with expression of the Citron homology domain.Mechanistically,the Citron homology domain acted as a dominant-negative mutant,impeding MAP4K-mediated phosphorylation of the dishevelled proteins and thereby controlling the Wnt/β-catenin pathway.These findings implicate a therapeutic potential of targeting MAP4Ks to alleviate the detrimental effects of traumatic brain injury.
      原文链接:
    • 万方数据
    • 维普

    Human neural stem cell-derived extracellular vesicles protect against ischemic stroke by activating the PI3K/AKT/mTOR pathway

    Jiayi WangMengke ZhaoDong FuMeina Wang...
    3245-3258页
    查看更多>>摘要：Human neural stem cell-derived extracellular vesicles exhibit analogous functions to their parental cells,and can thus be used as substitutes for stem cells in stem cell therapy,thereby mitigating the risks of stem cell therapy and advancing the frontiers of stem cell-derived treatments.This lays a foundation for the development of potentially potent new treatment modalities for ischemic stroke.However,the precise mechanisms underlying the efficacy and safety of human neural stem cell-derived extracellular vesicles remain unclear,presenting challenges for clinical translation.To promote the translation of therapy based on human neural stem cell-derived extracellular vesicles from the bench to the bedside,we conducted a comprehensive preclinical study to evaluate the efficacy and safety of human neural stem cell-derived extracellular vesicles in the treatment of ischemic stroke.We found that administration of human neural stem cell-derived extracellular vesicles to an ischemic stroke rat model reduced the volume of cerebral infarction and promoted functional recovery by alleviating neuronal apoptosis.The human neural stem cell-derived extracellular vesicles reduced neuronal apoptosis by enhancing phosphorylation of phosphoinositide 3-kinase,mammalian target of rapamycin,and protein kinase B,and these effects were reversed by treatment with a phosphoinositide 3-kinase inhibitor.These findings suggest that human neural stem cell-derived extracellular vesicles play a neuroprotective role in ischemic stroke through activation of phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway.Finally,we showed that human neural stem cell-derived extracellular vesicles have a good in vivo safety profile.Therefore,human neural stem cell-derived extracellular vesicles are a promising potential agent for the treatment of ischemic stroke.
      原文链接:
    • 万方数据
    • 维普

    Glutamatergic CYLD deletion leads to aberrant excitatory activity in the basolateral amygdala:association with enhanced cued fear expression

    Huidong LiFaqin LiZhaoyi ChenErwen Wu...
    3259-3272页
    查看更多>>摘要：Neuronal activity,synaptic transmission,and molecular changes in the basolateral amygdala play critical roles in fear memory.Cylindromatosis(CYLD)is a deubiquitinase that negatively regulates the nuclear factor kappa-B pathway.CYLD is well studied in non-neuronal cells,yet under-investigated in the brain,where it is highly expressed.Emerging studies have shown involvement of CYLD in the remodeling of glutamatergic synapses,neuroinflammation,fear memory,and anxiety-and autism-like behaviors.However,the precise role of CYLD in glutamatergic neurons is largely unknown.Here,we first proposed involvement of CYLD in cued fear expression.We next constructed transgenic model mice with specific deletion of Cyld from glutamatergic neurons.Our results show that glutamatergic CYLD deficiency exaggerated the expression of cued fear in only male mice.Further,loss of CYLD in glutamatergic neurons resulted in enhanced neuronal activation,impaired excitatory synaptic transmission,and altered levels of glutamate receptors accompanied by over-activation of microglia in the basolateral amygdala of male mice.Altogether,our study suggests a critical role of glutamatergic CYLD in maintaining normal neuronal,synaptic,and microglial activation.This may contribute,at least in part,to cued fear expression.
      原文链接:
    • 万方数据
    • 维普

    Exosomes originating from neural stem cells undergoing necroptosis participate in cellular communication by inducing TSC2 upregulation of recipient cells following spinal cord injury

    Shiming LiJianfeng LiGuoliang ChenTao Lin...
    3273-3286页
    查看更多>>摘要：We previously demonstrated that inhibiting neural stem cells necroptosis enhances functional recovery after spinal cord injury.While exosomes are recognized as playing a pivotal role in neural stem cells exocrine function,their precise function in spinal cord injury remains unclear.To investigate the role of exosomes generated following neural stem cells necroptosis after spinal cord injury,we conducted single-cell RNA sequencing and validated that neural stem cells originate from ependymal cells and undergo necroptosis in response to spinal cord injury.Subsequently,we established an in vitro necroptosis model using neural stem cells isolated from embryonic mice aged 16-17 days and extracted exosomes.The results showed that necroptosis did not significantly impact the fundamental characteristics or number of exosomes.Transcriptome sequencing of exosomes in necroptosis group identified 108 differentially expressed messenger RNAs,104 long non-coding RNAs,720 circular RNAs,and 14 microRNAs compared with the control group.Construction of a competing endogenous RNA network identified the following hub genes:tuberous sclerosis 2(Tsc2),solute carrier family 16 member 3(Slc16a3),and forkhead box protein P1(Foxp1).Notably,a significant elevation in TSC2 expression was observed in spinal cord tissues following spinal cord injury.TSC2-positive cells were localized around SRY-box transcription factor 2-positive cells within the injury zone.Furthermore,in vitro analysis revealed increased TSC2 expression in exosomal receptor cells compared with other cells.Further assessment of cellular communication following spinal cord injury showed that Tsc2 was involved in ependymal cellular communication at 1 and 3 days post-injury through the epidermal growth factor and midkine signaling pathways.In addition,Slc16a3 participated in cellular communication in ependymal cells at 7 days post-injury via the vascular endothelial growth factor and macrophage migration inhibitory factor signaling pathways.Collectively,these findings confirm that exosomes derived from neural stem cells undergoing necroptosis play an important role in cellular communication after spinal cord injury and induce TSC2 upregulation in recipient cells.
      原文链接:
    • 万方数据
    • 维普