首页期刊导航|中国神经再生研究（英文版）
期刊信息/Journal information
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

沈阳1234邮政信箱

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
正式出版
收录年代

    Exosomes:the next-generation therapeutic platform for ischemic stroke

    Wenjing YinHongyin MaYang QuJiaxin Ren...
    1221-1235页
    查看更多>>摘要：Current therapeutic strategies for ischemic stroke fall short of the desired objective of neurological functional recovery.Therefore,there is an urgent need to develop new methods for the treatment of this condition.Exosomes are natural cell-derived vesicles that mediate signal transduction between cells under physiological and pathological conditions.They have low immunogenicity,good stability,high delivery efficiency,and the ability to cross the blood-brain barrier.These physiological properties of exosomes have the potential to lead to new breakthroughs in the treatment of ischemic stroke.The rapid development of nanotechnology has advanced the application of engineered exosomes,which can effectively improve targeting ability,enhance therapeutic efficacy,and minimize the dosages needed.Advances in technology have also driven clinical translational research on exosomes.In this review,we describe the therapeutic effects of exosomes and their positive roles in current treatment strategies for ischemic stroke,including their anti-inflammation,anti-apoptosis,autophagy-regulation,angiogenesis,neurogenesis,and glial scar formation reduction effects.However,it is worth noting that,despite their significant therapeutic potential,there remains a dearth of standardized characterization methods and efficient isolation techniques capable of producing highly purified exosomes.Future optimization strategies should prioritize the exploration of suitable isolation techniques and the establishment of unified workflows to effectively harness exosomes for diagnostic or therapeutic applications in ischemic stroke.Ultimately,our review aims to summarize our understanding of exosome-based treatment prospects in ischemic stroke and foster innovative ideas for the development of exosome-based therapies.
      原文链接:
    • 万方数据
    • 维普

    NECAB family of neuronal calcium-binding proteins in health and disease

    Diones BuenoMichael K.E.SchäferSudena WangMichael J.Schmeisser...
    1236-1243页
    查看更多>>摘要：The N-terminal EF-hand calcium-binding proteins 1-3(NECAB1-3)constitute a family of predominantly neuronal proteins characterized by the presence of at least one EF-hand calcium-binding domain and a functionally less well characterized C-terminal antibiotic biosynthesis monooxygenase domain.All three family members were initially discovered due to their interactions with other proteins.NECAB1 associates with synaptotagmin-1,a critical neuronal protein involved in membrane trafficking and synaptic vesicle exocytosis.NECAB2 interacts with predominantly striatal G-protein-coupled receptors,while NECAB3 partners with amyloid-β A4 precursor protein-binding family A members 2 and 3,key regulators of amyloid-β production.This demonstrates the capacity of the family for interactions with various classes of proteins.NECAB proteins exhibit distinct subcellular localizations:NECAB1 is found in the nucleus and cytosol,NECAB2 resides in endosomes and the plasma membrane,and NECAB3 is present in the endoplasmic reticulum and Golgi apparatus.The antibiotic biosynthesis monooxygenase domain,an evolutionarily ancient component,is akin to atypical heme oxygenases in prokaryotes but is not well-characterized in vertebrates.Prokaryotic antibiotic biosynthesis monooxygenase domains typically form dimers,suggesting that calcium-mediated conformational changes in NECAB proteins may induce antibiotic biosynthesis monooxygenase domain dimerization,potentially activating some enzymatic properties.However,the substrate for this enzymatic activity remains uncertain.Alternatively,calcium-mediated conformational changes might influence protein interactions or the subcellular localization of NECAB proteins by controlling the availability of protein-protein interaction domains situated between the EF hands and the antibiotic biosynthesis monooxygenase domain.This review summarizes what is known about genomic organization,tissue expression,intracellular localization,interaction partners,and the physiological and pathophysiological role of the NECAB family.
      原文链接:
    • 万方数据
    • 维普

    The role of axon guidance molecules in the pathogenesis of epilepsy

    Zheng LiuChunhua PanHao Huang
    1244-1257页
    查看更多>>摘要：Current treatments for epilepsy can only manage the symptoms of the condition but cannot alter the initial onset or halt the progression of the disease.Consequently,it is crucial to identify drugs that can target novel cellular and molecular mechanisms and mechanisms of action.Increasing evidence suggests that axon guidance molecules play a role in the structural and functional modifications of neural networks and that the dysregulation of these molecules is associated with epilepsy susceptibility.In this review,we discuss the essential role of axon guidance molecules in neuronal activity in patients with epilepsy as well as the impact of these molecules on synaptic plasticity and brain tissue remodeling.Furthermore,we examine the relationship between axon guidance molecules and neuroinflammation,as well as the structural changes in specific brain regions that contribute to the development of epilepsy.Ample evidence indicates that axon guidance molecules,including semaphorins and ephrins,play a fundamental role in guiding axon growth and the establishment of synaptic connections.Deviations in their expression or function can disrupt neuronal connections,ultimately leading to epileptic seizures.The remodeling of neural networks is a significant characteristic of epilepsy,with axon guidance molecules playing a role in the dynamic reorganization of neural circuits.This,in turn,affects synapse formation and elimination.Dysregulation of these molecules can upset the delicate balance between excitation and inhibition within a neural network,thereby increasing the risk of overexcitation and the development of epilepsy.Inflammatory signals can regulate the expression and function of axon guidance molecules,thus influencing axonal growth,axon orientation,and synaptic plasticity.The dysregulation of neuroinflammation can intensify neuronal dysfunction and contribute to the occurrence of epilepsy.This review delves into the mechanisms associated with the pathogenicity of axon guidance molecules in epilepsy,offering a valuable reference for the exploration of therapeutic targets and presenting a fresh perspective on treatment strategies for this condition.
      原文链接:
    • 万方数据
    • 维普

    Potassium and calcium channels in different nerve cells act as therapeutic targets in neurological disorders

    Qing QiuMengting YangDanfeng GongHaiying Liang...
    1258-1276页
    查看更多>>摘要：The central nervous system,information integration center of the body,is mainly composed of neurons and glial cells.The neuron is one of the most basic and important structural and functional units of the central nervous system,with sensory stimulation and excitation conduction functions.Astrocytes and microglia belong to the glial cell family,which is the main source of cytokines and represents the main defense system of the central nervous system.Nerve cells undergo neurotransmission or gliotransmission,which regulates neuronal activity via the ion channels,receptors,or transporters expressed on nerve cell membranes.Ion channels,composed of large transmembrane proteins,play crucial roles in maintaining nerve cell homeostasis.These channels are also important for control of the membrane potential and in the secretion of neurotransmitters.A variety of cellular functions and life activities,including functional regulation of the central nervous system,the generation and conduction of nerve excitation,the occurrence of receptor potential,heart pulsation,smooth muscle peristalsis,skeletal muscle contraction,and hormone secretion,are closely related to ion channels associated with passive transmembrane transport.Two types of ion channels in the central nervous system,potassium channels and calcium channels,are closely related to various neurological disorders,including Alzheimer's disease,Parkinson's disease,and epilepsy.Accordingly,various drugs that can affect these ion channels have been explored deeply to provide new directions for the treatment of these neurological disorders.In this review,we focus on the functions of potassium and calcium ion channels in different nerve cells and their involvement in neurological disorders such as Parkinson's disease,Alzheimer's disease,depression,epilepsy,autism,and rare disorders.We also describe several clinical drugs that target potassium or calcium channels in nerve cells and could be used to treat these disorders.We concluded that there are few clinical drugs that can improve the pathology these diseases by acting on potassium or calcium ions.Although a few novel ion-channel-specific modulators have been discovered,meaningful therapies have largely not yet been realized.The lack of target-specific drugs,their requirement to cross the blood-brain barrier,and their exact underlying mechanisms all need further attention.This review aims to explain the urgent problems that need research progress and provide comprehensive information aiming to arouse the research community's interest in the development of ion channel-targeting drugs and the identification of new therapeutic targets for that can increase the cure rate of nervous system diseases and reduce the occurrence of adverse reactions in other systems.
      原文链接:
    • 万方数据
    • 维普

    T cell interactions with microglia in immune-inflammatory processes of ischemic stroke

    Yuxiao ZhengZilin RenYing LiuJuntang Yan...
    1277-1292页
    查看更多>>摘要：The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first immune cells to be activated after an ischemic stroke,microglia play an important immunomodulatory role in the progression of the condition.After an ischemic stroke,peripheral blood immune cells(mainly T cells)are recruited to the central nervous system by chemokines secreted by immune cells in the brain,where they interact with central nervous system cells(mainly microglia)to trigger a secondary neuroimmune response.This review summarizes the interactions between T cells and microglia in the immune-inflammatory processes of ischemic stroke.We found that,during ischemic stroke,T cells and microglia demonstrate a more pronounced synergistic effect.Th1,Th17,and M1 microglia can co-secrete pro-inflammatory factors,such as interferon-γ,tumor necrosis factor-α,and interleukin-1β,to promote neuroinflammation and exacerbate brain injury.Th2,Treg,and M2 microglia jointly secrete anti-inflammatory factors,such as interleukin-4,interleukin-10,and transforming growth factor-β,to inhibit the progression of neuroinflammation,as well as growth factors such as brain-derived neurotrophic factor to promote nerve regeneration and repair brain injury.Immune interactions between microglia and T cells influence the direction of the subsequent neuroinflammation,which in turn determines the prognosis of ischemic stroke patients.Clinical trials have been conducted on the ways to modulate the interactions between T cells and microglia toward anti-inflammatory communication using the immunosuppressant fingolimod or overdosing with Treg cells to promote neural tissue repair and reduce the damage caused by ischemic stroke.However,such studies have been relatively infrequent,and clinical experience is still insufficient.In summary,in ischemic stroke,T cell subsets and activated microglia act synergistically to regulate inflammatory progression,mainly by secreting inflammatory factors.In the future,a key research direction for ischemic stroke treatment could be rooted in the enhancement of anti-inflammatory factor secretion by promoting the generation of Th2 and Treg cells,along with the activation of M2-type microglia.These approaches may alleviate neuroinflammation and facilitate the repair of neural tissues.
      原文链接:
    • 万方数据
    • 维普

    Combinatorial therapies for spinal cord injury repair

    Carla S.SousaAndreia MonteiroAntónio J.SalgadoNuno A.Silva...
    1293-1308页
    查看更多>>摘要：Spinal cord injuries have profound detrimental effects on individuals,regardless of whether they are caused by trauma or non-traumatic events.The compromised regeneration of the spinal cord is primarily attributed to damaged neurons,inhibitory molecules,dysfunctional immune response,and glial scarring.Unfortunately,currently,there are no effective treatments available that can fully repair the spinal cord and improve functional outcomes.Nevertheless,numerous pre-clinical approaches have been studied for spinal cord injury recovery,including using biomaterials,cells,drugs,or technological-based strategies.Combinatorial treatments,which target various aspects of spinal cord injury pathophysiology,have been extensively tested in the last decade.These approaches aim to synergistically enhance repair processes by addressing various obstacles faced during spinal cord regeneration.Thus,this review intends to provide scientists and clinicians with an overview of pre-clinical combinatorial approaches that have been developed toward the solution of spinal cord regeneration as well as update the current knowledge about spinal cord injury pathophysiology with an emphasis on the current clinical management.
      原文链接:
    • 万方数据
    • 维普

    The complex effects of miR-146a in the pathogenesis of Alzheimer's disease

    Yunfan LongJiajia LiuYu WangHaidong Guo...
    1309-1323页
    查看更多>>摘要：Alzheimer's disease is a neurodegenerative disorder characterized by cognitive dysfunction and behavioral abnormalities.Neuroinflammatory plaques formed through the extracellular deposition of amyloid-β proteins,as well as neurofibrillary tangles formed by the intracellular deposition of hyperphosphorylated tau proteins,comprise two typical pathological features of Alzheimer's disease.Besides symptomatic treatment,there are no effective therapies for delaying Alzheimer's disease progression.MicroRNAs(miR)are small,non-coding RNAs that negatively regulate gene expression at the transcriptional and translational levels and play important roles in multiple physiological and pathological processes.Indeed,miR-146a,a NF-κB-regulated gene,has been extensively implicated in the development of Alzheimer's disease through several pathways.Research has demonstrated substantial dysregulation of miR-146a both during the initial phases and throughout the progression of this disorder.MiR-146a is believed to reduce amyloid-β deposition and tau protein hyperphosphorylation through the TLR/IRAK1/TRAF6 pathway;however,there is also evidence supporting that it can promote these processes through many other pathways,thus exacerbating the pathological manifestations of Alzheimer's disease.It has been widely reported that miR-146a mediates synaptic dysfunction,mitochondrial dysfunction,and neuronal death by targeting mRNAs encoding synaptic-related proteins,mitochondrial-related proteins,and membrane proteins,as well as other mRNAs.Regarding the impact on glial cells,miR-146a also exhibits differential effects.On one hand,it causes widespread and sustained inflammation through certain pathways,while on the other hand,it can reverse the polarization of astrocytes and microglia,alleviate neuroinflammation,and promote oligodendrocyte progenitor cell differentiation,thus maintaining the normal function of the myelin sheath and exerting a protective effect on neurons.In this review,we provide a comprehensive analysis of the involvement of miR-146a in the pathogenesis of Alzheimer's disease.We aim to elucidate the relationship between miR-146a and the key pathological manifestations of Alzheimer's disease,such as amyloid-β deposition,tau protein hyperphosphorylation,neuronal death,mitochondrial dysfunction,synaptic dysfunction,and glial cell dysfunction,as well as summarize recent relevant studies that have highlighted the potential of miR-146a as a clinical diagnostic marker and therapeutic target for Alzheimer's disease.
      原文链接:
    • 万方数据

    Complement-dependent neuroinflammation in spinal cord injury:from pathology to therapeutic implications

    Hassan SaadBachar El BabaAli TfailyFiras Kobeissy...
    1324-1335页
    查看更多>>摘要：Spinal cord injury remains a major cause of disability in young adults,and beyond acute decompression and rehabilitation,there are no pharmacological treatments to limit the progression of injury and optimize recovery in this population.Following the thorough investigation of the complement system in triggering and propagating cerebral neuroinflammation,a similar role for complement in spinal neuroinflammation is a focus of ongoing research.In this work,we survey the current literature investigating the role of complement in spinal cord injury including the sources of complement proteins,triggers of complement activation,and role of effector functions in the pathology.We study relevant data demonstrating the different triggers of complement activation after spinal cord injury including direct binding to cellular debris,and or activation via antibody binding to damage-associated molecular patterns.Several effector functions of complement have been implicated in spinal cord injury,and we critically evaluate recent studies on the dual role of complement anaphylatoxins in spinal cord injury while emphasizing the lack of pathophysiological understanding of the role of opsonins in spinal cord injury.Following this pathophysiological review,we systematically review the different translational approaches used in preclinical models of spinal cord injury and discuss the challenges for future translation into human subjects.This review emphasizes the need for future studies to dissect the roles of different complement pathways in the pathology of spinal cord injury,to evaluate the phases of involvement of opsonins and anaphylatoxins,and to study the role of complement in white matter degeneration and regeneration using translational strategies to supplement genetic models.
      原文链接:
    • 万方数据
    • 维普

    Heterogeneity of mature oligodendrocytes in the central nervous system

    Chao WengAdam M.R.GrohMoein YaqubiQiao-Ling Cui...
    1336-1349页
    查看更多>>摘要：Mature oligodendrocytes form myelin sheaths that are crucial for the insulation of axons and efficient signal transmission in the central nervous system.Recent evidence has challenged the classical view of the functionally static mature oligodendrocyte and revealed a gamut of dynamic functions such as the ability to modulate neuronal circuitry and provide metabolic support to axons.Despite the recognition of potential heterogeneity in mature oligodendrocyte function,a comprehensive summary of mature oligodendrocyte diversity is lacking.We delve into early 20th-century studies by Robertson and Río-Hortega that laid the foundation for the modern identification of regional and morphological heterogeneity in mature oligodendrocytes.Indeed,recent morphologic and functional studies call into question the long-assumed homogeneity of mature oligodendrocyte function through the identification of distinct subtypes with varying myelination preferences.Furthermore,modern molecular investigations,employing techniques such as single cell/nucleus RNA sequencing,consistently unveil at least six mature oligodendrocyte subpopulations in the human central nervous system that are highly transcriptomically diverse and vary with central nervous system region.Age and disease related mature oligodendrocyte variation denotes the impact of pathological conditions such as multiple sclerosis,Alzheimer's disease,and psychiatric disorders.Nevertheless,caution is warranted when subclassifying mature oligodendrocytes because of the simplification needed to make conclusions about cell identity from temporally confined investigations.Future studies leveraging advanced techniques like spatial transcriptomics and single-cell proteomics promise a more nuanced understanding of mature oligodendrocyte heterogeneity.Such research avenues that precisely evaluate mature oligodendrocyte heterogeneity with care to understand the mitigating influence of species,sex,central nervous system region,age,and disease,hold promise for the development of therapeutic interventions targeting varied central nervous system pathology.
      原文链接:
    • 万方数据
    • 维普

    Decoding the nexus:branched-chain amino acids and their connection with sleep,circadian rhythms,and cardiometabolic health

    Hui LiLaurent Seugnet
    1350-1363页
    查看更多>>摘要：The sleep-wake cycle stands as an integrative process essential for sustaining optimal brain function and,either directly or indirectly,overall body health,encompassing metabolic and cardiovascular well-being.Given the heightened metabolic activity of the brain,there exists a considerable demand for nutrients in comparison to other organs.Among these,the branched-chain amino acids,comprising leucine,isoleucine,and valine,display distinctive significance,from their contribution to protein structure to their involvement in overall metabolism,especially in cerebral processes.Among the first amino acids that are released into circulation post-food intake,branched-chain amino acids assume a pivotal role in the regulation of protein synthesis,modulating insulin secretion and the amino acid sensing pathway of target of rapamycin.Branched-chain amino acids are key players in influencing the brain's uptake of monoamine precursors,competing for a shared transporter.Beyond their involvement in protein synthesis,these amino acids contribute to the metabolic cycles of γ-aminobutyric acid and glutamate,as well as energy metabolism.Notably,they impact GABAergic neurons and the excitation/inhibition balance.The rhythmicity of branched-chain amino acids in plasma concentrations,observed over a 24-hour cycle and conserved in rodent models,is under circadian clock control.The mechanisms underlying those rhythms and the physiological consequences of their disruption are not fully understood.Disturbed sleep,obesity,diabetes,and cardiovascular diseases can elevate branched-chain amino acid concentrations or modify their oscillatory dynamics.The mechanisms driving these effects are currently the focal point of ongoing research efforts,since normalizing branched-chain amino acid levels has the ability to alleviate the severity of these pathologies.In this context,the Drosophila model,though underutilized,holds promise in shedding new light on these mechanisms.Initial findings indicate its potential to introduce novel concepts,particularly in elucidating the intricate connections between the circadian clock,sleep/wake,and metabolism.Consequently,the use and transport of branched-chain amino acids emerge as critical components and orchestrators in the web of interactions across multiple organs throughout the sleep/wake cycle.They could represent one of the so far elusive mechanisms connecting sleep patterns to metabolic and cardiovascular health,paving the way for potential therapeutic interventions.
      原文链接:
    • 万方数据
    • 维普