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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

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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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    Harnessing therapeutic potential of induced pluripotent stem cell-derived endothelial cells for remyelination in the central nervous system

    Dan MaNona Pop
    1715-1716页
      原文链接:
    • 万方数据

    Insights from an academic endeavor into central nervous system drug discovery

    Lieve van VeggelAn M.VoetsTim VanmierloRudy Schreiber...
    1717-1718页
      原文链接:
    • 万方数据
    • 维普

    Remaking a connection:molecular players involved in post-injury synapse formation

    Diogo ToméRamiro D.Almeida
    1719-1720页
      原文链接:
    • 万方数据
    • 维普

    Increased excitatory amino acid transporter 2 levels in basolateral amygdala astrocytes mediate chronic stress-induced anxiety-like behavior

    Xirong XuShoumin XuanShuai ChenDan Liu...
    1721-1734页
    查看更多>>摘要：The conventional perception of astrocytes as mere supportive cells within the brain has recently been called into question by empirical evidence,which has revealed their active involvement in regulating brain function and encoding behaviors associated with emotions.Specifically,astrocytes in the basolateral amygdala have been found to play a role in the modulation of anxiety-like behaviors triggered by chronic stress.Nevertheless,the precise molecular mechanisms by which basolateral amygdala astrocytes regulate chronic stress-induced anxiety-like behaviors remain to be fully elucidated.In this study,we found that in a mouse model of anxiety triggered by unpredictable chronic mild stress,the expression of excitatory amino acid transporter 2 was upregulated in the basolateral amygdala.Interestingly,our findings indicate that the targeted knockdown of excitatory amino acid transporter 2 specifically within the basolateral amygdala astrocytes was able to rescue the anxiety-like behavior in mice subjected to stress.Furthermore,we found that the overexpression of excitatory amino acid transporter 2 in the basolateral amygdala,whether achieved through intracranial administration of excitatory amino acid transporter 2 agonists or through injection of excitatory amino acid transporter 2-overexpressing viruses with GfaABC1D promoters,evoked anxiety-like behavior in mice.Our single-nucleus RNA sequencing analysis further confirmed that chronic stress induced an upregulation of excitatory amino acid transporter 2 specifically in astrocytes in the basolateral amygdala.Moreover,through in vivo calcium signal recordings,we found that the frequency of calcium activity in the basolateral amygdala of mice subjected to chronic stress was higher compared with normal mice.After knocking down the expression of excitatory amino acid transporter 2 in the basolateral amygdala,the frequency of calcium activity was not significantly increased,and anxiety-like behavior was obviously mitigated.Additionally,administration of an excitatory amino acid transporter 2 inhibitor in the basolateral amygdala yielded a notable reduction in anxiety level among mice subjected to stress.These results suggest that basolateral amygdala astrocytic excitatory amino acid transporter 2 plays a role in in the regulation of unpredictable chronic mild stress-induced anxiety-like behavior by impacting the activity of local glutamatergic neurons,and targeting excitatory amino acid transporter 2 in the basolateral amygdala holds therapeutic promise for addressing anxiety disorders.
      原文链接:
    • 万方数据

    Dip2a regulates stress susceptibility in the basolateral amygdala

    Jing LiZixuan HeWeitai ChaiMeng Tian...
    1735-1748页
    查看更多>>摘要：Dysregulation of neurotransmitter metabolism in the central nervous system contributes to mood disorders such as depression,anxiety,and post-traumatic stress disorder.Monoamines and amino acids are important types of neurotransmitters.Our previous results have shown that disco-interacting protein 2 homolog A(Dip2a)knockout mice exhibit brain development disorders and abnormal amino acid metabolism in serum.This suggests that DIP2A is involved in the metabolism of amino acid-associated neurotransmitters.Therefore,we performed targeted neurotransmitter metabolomics analysis and found that Dip2a deficiency caused abnormal metabolism of tryptophan and thyroxine in the basolateral amygdala and medial prefrontal cortex.In addition,acute restraint stress induced a decrease in 5-hydroxytryptamine in the basolateral amygdala.Additionally,Dip2a was abundantly expressed in excitatory neurons of the basolateral amygdala,and deletion of Dip2a in these neurons resulted in hopelessness-like behavior in the tail suspension test.Altogether,these findings demonstrate that DIP2A in the basolateral amygdala may be involved in the regulation of stress susceptibility.This provides critical evidence implicating a role of DIP2A in affective disorders.
      原文链接:
    • 万方数据
    • 维普

    Enhancing m6A modification in the motor cortex facilitates corticospinal tract remodeling after spinal cord injury

    Tian QinYuxin JinYiming QinFeifei Yuan...
    1749-1763页
    查看更多>>摘要：Spinal cord injury typically causes corticospinal tract disruption.Although the disrupted corticospinal tract can self-regenerate to a certain degree,the underlying mechanism of this process is still unclear.N6-methyladenosine(m6A)modifications are the most common form of epigenetic regulation at the RNA level and play an essential role in biological processes.However,whether m6A modifications participate in corticospinal tract regeneration after spinal cord injury remains unknown.We found that expression of methyltransferase 14 protein(METTL14)in the locomotor cortex was high after spinal cord injury and accompanied by elevated m6A levels.Knockdown of Mettl14 in the locomotor cortex was not favorable for corticospinal tract regeneration and neurological recovery after spinal cord injury.Through bioinformatics analysis and methylated RNA immunoprecipitation-quantitative polymerase chain reaction,we found that METTL14 regulated Trib2 expression in an m6A-regulated manner,thereby activating the mitogen-activated protein kinase pathway and promoting corticospinal tract regeneration.Finally,we administered syringin,a stabilizer of METTL14,using molecular docking.Results confirmed that syringin can promote corticospinal tract regeneration and facilitate neurological recovery by stabilizing METTL14.Findings from this study reveal that m6A modification is involved in the regulation of corticospinal tract regeneration after spinal cord injury.
      原文链接:
    • 万方数据

    Peripheral blood RNA biomarkers can predict lesion severity in degenerative cervical myelopathy

    Zhenzhong ZhengJialin ChenJinghong XuBin Jiang...
    1764-1775页
    查看更多>>摘要：Degenerative cervical myelopathy is a common cause of spinal cord injury,with longer symptom duration and higher myelopathy severity indicating a worse prognosis.While numerous studies have investigated serological biomarkers for acute spinal cord injury,few studies have explored such biomarkers for diagnosing degenerative cervical myelopathy.This study involved 30 patients with degenerative cervical myelopathy(51.3±7.3 years old,12 women and 18 men),seven healthy controls(25.7±1.7 years old,one woman and six men),and nine patients with cervical spondylotic radiculopathy(51.9±8.6 years old,three women and six men).Analysis of blood samples from the three groups showed clear differences in transcriptomic characteristics.Enrichment analysis identified 128 differentially expressed genes that were enriched in patients with neurological disabilities.Using least absolute shrinkage and selection operator analysis,we constructed a five-gene model(TBCD,TPM2,PNKD,EIF4G2,and AP5Z1)to diagnose degenerative cervical myelopathy with an accuracy of 93.5％.One-gene models(TCAP and SDHA)identified mild and severe degenerative cervical myelopathy with accuracies of 83.3％and 76.7％,respectively.Signatures of two immune cell types(memory B cells and memory-activated CD4+T cells)predicted levels of lesions in degenerative cervical myelopathy with 80％accuracy.Our results suggest that peripheral blood RNA biomarkers could be used to predict lesion severity in degenerative cervical myelopathy.
      原文链接:
    • 万方数据
    • 维普

    Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

    Zige JiangDexiang LiuTingting LiChengcheng Gai...
    1776-1788页
    查看更多>>摘要：The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid.Quinolinic acid accumulation results in oxidative stress,which leads to neurotoxicity.However,the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown.In this study,we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice,respectively.We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum,which was accompanied by down-regulation of cystathionine β-synthase,an enzyme responsible for hydrogen sulfide production.However,treatment with NaHS(a hydrogen sulfide donor)increased hydrogen sulfide levels in the neurons and in mouse serum,as well as cystathionine β-synthase expression in the neurons and the mouse striatum,while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum.These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression.Finally,treatment with the nuclear factor erythroid 2-related factor 2 inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress.Taken together,our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.
      原文链接:
    • 万方数据

    Silk-based nerve guidance conduits with macroscopic holes modulate the vascularization of regenerating rat sciatic nerve

    Carina HromadaPatrick HeimelMarkus KerblLászló Gál...
    1789-1800页
    查看更多>>摘要：Peripheral nerve injuries induce a severe motor and sensory deficit.Since the availability of autologous nerve transplants for nerve repair is very limited,alternative treatment strategies are sought,including the use of tubular nerve guidance conduits(tNGCs).However,the use of tNGCs results in poor functional recovery and central necrosis of the regenerating tissue,which limits their application to short nerve lesion defects(typically shorter than 3 cm).Given the importance of vascularization in nerve regeneration,we hypothesized that enabling the growth of blood vessels from the surrounding tissue into the regenerating nerve within the tNGC would help eliminate necrotic processes and lead to improved regeneration.In this study,we reported the application of macroscopic holes into the tubular walls of silk-based tNGCs and compared the various features of these improved si l k+tNGCs with the tubes without holes(silk-tNGCs)and autologous nerve transplants in an 8-mm sciatic nerve defect in rats.Using a combination of micro-computed tomography and histological analyses,we were able to prove that the use of silk+tNGCs induced the growth of blood vessels from the adjacent tissue to the intraluminal neovascular formation.A significantly higher number of blood vessels in the silk+group was found compared with autologous nerve transplants and silk-,accompanied by improved axon regeneration at the distal coaptation point compared with the silk-tNGCs at 7 weeks postoperatively.In the 15-mm(critical size)sciatic nerve defect model,we again observed a distinct ingrowth of blood vessels through the tubular walls of si l k+tNGCs,but without improved functional recovery at 12 weeks postoperatively.Our data proves that macroporous tNGCs increase the vascular supply of regenerating nerves and facilitate improved axonal regeneration in a short-defect model but not in a critical-size defect model.This study suggests that further optimization of the macroscopic holes silk+tNGC approach containing macroscopic holes might result in improved grafting technology suitable for future clinical use.
      原文链接:
    • 万方数据
    • 维普

    Characteristic changes in astrocyte properties during astrocyte-to-neuron conversion induced by NeuroD1/Ascl1/Dlx2

    Qing HeZhen WangYuchen WangMengjie Zhu...
    1801-1815页
    查看更多>>摘要：Direct in vivo conversion of astrocytes into functional new neurons induced by neural transcription factors has been recognized as a potential new therapeutic intervention for neural injury and degenerative disorders.However,a few recent studies have claimed that neural transcription factors cannot convert astrocytes into neurons,attributing the converted neurons to pre-existing neurons mis-expressing transgenes.In this study,we overexpressed three distinct neural transcription factors—NeuroD1,Ascl1,and Dlx2—in reactive astrocytes in mouse cortices subjected to stab injury,resulting in a series of significant changes in astrocyte properties.Initially,the three neural transcription factors were exclusively expressed in the nuclei of astrocytes.Over time,however,these astrocytes gradually adopted neuronal morphology,and the neural transcription factors was gradually observed in the nuclei of neuron-like cells instead of astrocytes.Furthermore,we noted that transcription factor-infected astrocytes showed a progressive decrease in the expression of astrocytic markers AQP4(astrocyte endfeet signal),CX43(gap junction signal),and S100β.Importantly,none of these changes could be attributed to transgene leakage into pre-existing neurons.Therefore,our findings suggest that neural transcription factors such as NeuroD1,Ascl1,and Dlx2 can effectively convert reactive astrocytes into neurons in the adult mammalian brain.
      原文链接:
    • 万方数据
    • 维普