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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

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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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    Single-cell and spatial omics:exploring hypothalamic heterogeneity

    Muhammad JunaidEun Jeong LeeSu Bin Lim
    1525-1540页
    查看更多>>摘要：Elucidating the complex dynamic cellular organization in the hypothalamus is critical for understanding its role in coordinating fundamental body functions.Over the past decade,single-cell and spatial omics technologies have significantly evolved,overcoming initial technical challenges in capturing and analyzing individual cells.These high-throughput omics technologies now offer a remarkable opportunity to comprehend the complex spatiotemporal patterns of transcriptional diversity and cell-type characteristics across the entire hypothalamus.Current single-cell and single-nucleus RNA sequencing methods comprehensively quantify gene expression by exploring distinct phenotypes across various subregions of the hypothalamus.However,single-cell/single-nucleus RNA sequencing requires isolating the cell/nuclei from the tissue,potentially resulting in the loss of spatial information concerning neuronal networks.Spatial transcriptomics methods,by bypassing the cell dissociation,can elucidate the intricate spatial organization of neural networks through their imaging and sequencing technologies.In this review,we highlight the applicative value of single-cell and spatial transcriptomics in exploring the complex molecular-genetic diversity of hypothalamic cell types,driven by recent high-throughput achievements.
      原文链接:
    • 万方数据
    • 维普

    Peripheral mitochondrial DNA as a neuroinflammatory biomarker for major depressive disorder

    Jinmei YeCong DuanJiaxin HanJinrong Chen...
    1541-1554页
    查看更多>>摘要：In the pathogenesis of major depressive disorder,chronic stress-related neuroinflammation hinders favorable prognosis and antidepressant response.Mitochondrial DNA may be an inflammatory trigger,after its release from stress-induced dysfunctional central nervous system mitochondria into peripheral circulation.This evidence supports the potential use of peripheral mitochondrial DNA as a neuroinflammatory biomarker for the diagnosis and treatment of major depressive disorder.Herein,we critically review the neuroinflammation theory in major depressive disorder,providing compelling evidence that mitochondrial DNA release acts as a critical biological substrate,and that it constitutes the neuroinflammatory disease pathway.After its release,mitochondrial DNA can be carried in the exosomes and transported to extracellular spaces in the central nervous system and peripheral circulation.Detectable exosomes render encaged mitochondrial DNA relatively stable.This mitochondrial DNA in peripheral circulation can thus be directly detected in clinical practice.These characteristics illustrate the potential for mitochondrial DNA to serve as an innovative clinical biomarker and molecular treatment target for major depressive disorder.This review also highlights the future potential value of clinical applications combining mitochondrial DNA with a panel of other biomarkers,to improve diagnostic precision in major depressive disorder.
      原文链接:
    • 万方数据
    • 维普

    Therapeutic potential of exercise-hormone irisin in Alzheimer's disease

    Eunhee KimRudolph E.TanziSe Hoon Choi
    1555-1564页
    查看更多>>摘要：Irisin is a myokine that is generated by cleavage of the membrane protein fibronectin typeⅢ domain-containing protein 5(FNDC5)in response to physical exercise.Studies reveal that irisin/FNDC5 has neuroprotective functions against Alzheimer's disease,the most common form of dementia in the elderly,by improving cognitive function and reducing amyloid-β and tau pathologies as well as neuroinflammation in cell culture or animal models of Alzheimer's disease.Although current and ongoing studies on irisin/FNDC5 show promising results,further mechanistic studies are required to clarify its potential as a meaningful therapeutic target for alleviating Alzheimer's disease.We recently found that irisin treatment reduces amyloid-β pathology by increasing the activity/levels of amyloid-β-degrading enzyme neprilysin secreted from astrocytes.Herein,we present an overview of irisin/FNDC5's protective roles and mechanisms against Alzheimer's disease.
      原文链接:
    • 万方数据

    Neurogenesis dynamics in the olfactory bulb:deciphering circuitry organization,function,and adaptive plasticity

    Moawiah M.Naffaa
    1565-1581页
    查看更多>>摘要：Adult neurogenesis persists after birth in the subventricular zone,with new neurons migrating to the granule cell layer and glomerular layers of the olfactory bulb,where they integrate into existing circuitry as inhibitory interneurons.The generation of these new neurons in the olfactory bulb supports both structural and functional plasticity,aiding in circuit remodeling triggered by memory and learning processes.However,the presence of these neurons,coupled with the cellular diversity within the olfactory bulb,presents an ongoing challenge in understanding its network organization and function.Moreover,the continuous integration of new neurons in the olfactory bulb plays a pivotal role in regulating olfactory information processing.This adaptive process responds to changes in epithelial composition and contributes to the formation of olfactory memories by modulating cellular connectivity within the olfactory bulb and interacting intricately with higher-order brain regions.The role of adult neurogenesis in olfactory bulb functions remains a topic of debate.Nevertheless,the functionality of the olfactory bulb is intricately linked to the organization of granule cells around mitral and tufted cells.This organizational pattern significantly impacts output,network behavior,and synaptic plasticity,which are crucial for olfactory perception and memory.Additionally,this organization is further shaped by axon terminals originating from cortical and subcortical regions.Despite the crucial role of olfactory bulb in brain functions and behaviors related to olfaction,these complex and highly interconnected processes have not been comprehensively studied as a whole.Therefore,this manuscript aims to discuss our current understanding and explore how neural plasticity and olfactory neurogenesis contribute to enhancing the adaptability of the olfactory system.These mechanisms are thought to support olfactory learning and memory,potentially through increased complexity and restructuring of neural network structures,as well as the addition of new granule granule cells that aid in olfactory adaptation.Additionally,the manuscript underscores the importance of employing precise methodologies to elucidate the specific roles of adult neurogenesis amidst conflicting data and varying experimental paradigms.Understanding these processes is essential for gaining insights into the complexities of olfactory function and behavior.
      原文链接:
    • 万方数据

    The complex roles of m6A modifications in neural stem cell proliferation,differentiation,and self-renewal and implications for memory and neurodegenerative diseases

    Yanxi LiJing XueYuejia MaKe Ye...
    1582-1598页
    查看更多>>摘要：N6-methyladenosine(m6A),the most prevalent and conserved RNA modification in eukaryotic cells,profoundly influences virtually all aspects of mRNA metabolism.mRNA plays crucial roles in neural stem cell genesis and neural regeneration,where it is highly concentrated and actively involved in these processes.Changes in m6A modification levels and the expression levels of related enzymatic proteins can lead to neurological dysfunction and contribute to the development of neurological diseases.Furthermore,the proliferation and differentiation of neural stem cells,as well as nerve regeneration,are intimately linked to memory function and neurodegenerative diseases.This paper presents a comprehensive review of the roles of m6A in neural stem cell proliferation,differentiation,and self-renewal,as well as its implications in memory and neurodegenerative diseases.m6A has demonstrated divergent effects on the proliferation and differentiation of neural stem cells.These observed contradictions may arise from the time-specific nature of m6A and its differential impact on neural stem cells across various stages of development.Similarly,the diverse effects of m6A on distinct types of memory could be attributed to the involvement of specific brain regions in memory formation and recall.Inconsistencies in m6A levels across different models of neurodegenerative disease,particularly Alzheimer's disease and Parkinson's disease,suggest that these disparities are linked to variations in the affected brain regions.Notably,the opposing changes in m6A levels observed in Parkinson's disease models exposed to manganese compared to normal Parkinson's disease models further underscore the complexity of m6A's role in neurodegenerative processes.The roles of m6A in neural stem cell proliferation,differentiation,and self-renewal,and its implications in memory and neurodegenerative diseases,appear contradictory.These inconsistencies may be attributed to the time-specific nature of m6A and its varying effects on distinct brain regions and in different environments.
      原文链接:
    • 万方数据

    Potential role of tanycyte-derived neurogenesis in Alzheimer's disease

    Guibo QiHan TangJianian HuSiying Kang...
    1599-1612页
    查看更多>>摘要：Tanycytes,specialized ependymal cells located in the hypothalamus,play a crucial role in the generation of new neurons that contribute to the neural circuits responsible for regulating the systemic energy balance.The precise coordination of the gene networks controlling neurogenesis in naive and mature tanycytes is essential for maintaining homeostasis in adulthood.However,our understanding of the molecular mechanisms and signaling pathways that govern the proliferation and differentiation of tanycytes into neurons remains limited.This article aims to review the recent advancements in research into the mechanisms and functions of tanycyte-derived neurogenesis.Studies employing lineage-tracing techniques have revealed that the neurogenesis specifically originating from tanycytes in the hypothalamus has a compensatory role in neuronal loss and helps maintain energy homeostasis during metabolic diseases.Intriguingly,metabolic disorders are considered early biomarkers of Alzheimer's disease.Furthermore,the neurogenic potential of tanycytes and the state of newborn neurons derived from tanycytes heavily depend on the maintenance of mild microenvironments,which may be disrupted in Alzheimer's disease due to the impaired blood-brain barrier function.However,the specific alterations and regulatory mechanisms governing tanycyte-derived neurogenesis in Alzheimer's disease remain unclear.Accumulating evidence suggests that tanycyte-derived neurogenesis might be impaired in Alzheimer's disease,exacerbating neurodegeneration.Confirming this hypothesis,however,poses a challenge because of the lack of long-term tracing and nucleus-specific analyses of newborn neurons in the hypothalamus of patients with Alzheimer's disease.Further research into the molecular mechanisms underlying tanycyte-derived neurogenesis holds promise for identifying small molecules capable of restoring tanycyte proliferation in neurodegenerative diseases.This line of investigation could provide valuable insights into potential therapeutic strategies for Alzheimer's disease and related conditions.
      原文链接:
    • 万方数据

    The potential mechanism and clinical application value of remote ischemic conditioning in stroke

    Yajun ZhuXiaoguo LiXingwei LeiLiuyang Tang...
    1613-1627页
    查看更多>>摘要：Some studies have confirmed the neuroprotective effect of remote ischemic conditioning against stroke.Although numerous animal researches have shown that the neuroprotective effect of remote ischemic conditioning may be related to neuroinflammation,cellular immunity,apoptosis,and autophagy,the exact underlying molecular mechanisms are unclear.This review summarizes the current status of different types of remote ischemic conditioning methods in animal and clinical studies and analyzes their commonalities and differences in neuroprotective mechanisms and signaling pathways.Remote ischemic conditioning has emerged as a potential therapeutic approach for improving stroke-induced brain injury owing to its simplicity,non-invasiveness,safety,and patient tolerability.Different forms of remote ischemic conditioning exhibit distinct intervention patterns,timing,and application range.Mechanistically,remote ischemic conditioning can exert neuroprotective effects by activating the Notch1/phosphatidylinositol 3-kinase/Akt signaling pathway,improving cerebral perfusion,suppressing neuroinflammation,inhibiting cell apoptosis,activating autophagy,and promoting neural regeneration.While remote ischemic conditioning has shown potential in improving stroke outcomes,its full clinical translation has not yet been achieved.
      原文链接:
    • 万方数据
    • 维普

    Role of the globus pallidus in motor and non-motor symptoms of Parkinson's disease

    Yimiao JiangZengxin QiHuixian ZhuKangli Shen...
    1628-1643页
    查看更多>>摘要：The globus pallidus plays a pivotal role in the basal ganglia circuit.Parkinson's disease is characterized by degeneration of dopamine-producing cells in the substantia nigra,which leads to dopamine deficiency in the brain that subsequently manifests as various motor and non-motor symptoms.This review aims to summarize the involvement of the globus pallidus in both motor and non-motor manifestations of Parkinson's disease.The firing activities of parvalbumin neurons in the medial globus pallidus,including both the firing rate and pattern,exhibit strong correlations with the bradykinesia and rigidity associated with Parkinson's disease.Increased beta oscillations,which are highly correlated with bradykinesia and rigidity,are regulated by the lateral globus pallidus.Furthermore,bradykinesia and rigidity are strongly linked to the loss of dopaminergic projections within the cortical-basal ganglia-thalamocortical loop.Resting tremors are attributed to the transmission of pathological signals from the basal ganglia through the motor cortex to the cerebellum-ventral intermediate nucleus circuit.The cortico-striato-pallidal loop is responsible for mediating pallidi-associated sleep disorders.Medication and deep brain stimulation are the primary therapeutic strategies addressing the globus pallidus in Parkinson's disease.Medication is the primary treatment for motor symptoms in the early stages of Parkinson's disease,while deep brain stimulation has been clinically proven to be effective in alleviating symptoms in patients with advanced Parkinson's disease,particularly for the movement disorders caused by levodopa.Deep brain stimulation targeting the globus pallidus internus can improve motor function in patients with tremor-dominant and non-tremor-dominant Parkinson's disease,while deep brain stimulation targeting the globus pallidus externus can alter the temporal pattern of neural activity throughout the basal ganglia-thalamus network.Therefore,the composition of the globus pallidus neurons,the neurotransmitters that act on them,their electrical activity,and the neural circuits they form can guide the search for new multi-target drugs to treat Parkinson's disease in clinical practice.Examining the potential intra-nuclear and neural circuit mechanisms of deep brain stimulation associated with the globus pallidus can facilitate the management of both motor and non-motor symptoms while minimizing the side effects caused by deep brain stimulation.
      原文链接:
    • 万方数据

    Inflammasome links traumatic brain injury,chronic traumatic encephalopathy,and Alzheimer's disease

    Gabriela SeplovichYazan BouchiJuan Pablo de Rivero VaccariJennifer C.Munoz Pareja...
    1644-1664页
    查看更多>>摘要：Traumatic brain injury,chronic traumatic encephalopathy,and Alzheimer's disease are three distinct neurological disorders that share common pathophysiological mechanisms involving neuroinflammation.One sequela of neuroinflammation includes the pathologic hyperphosphorylation of tau protein,an endogenous microtubule-associated protein that protects the integrity of neuronal cytoskeletons.Tau hyperphosphorylation results in protein misfolding and subsequent accumulation of tau tangles forming neurotoxic aggregates.These misfolded proteins are characteristic of traumatic brain injury,chronic traumatic encephalopathy,and Alzheimer's disease and can lead to downstream neuroinflammatory processes,including assembly and activation of the inflammasome complex.Inflammasomes refer to a family of multimeric protein units that,upon activation,release a cascade of signaling molecules resulting in caspase-induced cell death and inflammation mediated by the release of interleukin-1β cytokine.One specific inflammasome,the NOD-like receptor protein 3,has been proposed to be a key regulator of tau phosphorylation where it has been shown that prolonged NOD-like receptor protein 3 activation acts as a causal factor in pathological tau accumulation and spreading.This review begins by describing the epidemiology and pathophysiology of traumatic brain injury,chronic traumatic encephalopathy,and Alzheimer's disease.Next,we highlight neuroinflammation as an overriding theme and discuss the role of the NOD-like receptor protein 3 inflammasome in the formation of tau deposits and how such tauopathic entities spread throughout the brain.We then propose a novel framework linking traumatic brain injury,chronic traumatic encephalopathy,and Alzheimer's disease as inflammasome-dependent pathologies that exist along a temporal continuum.Finally,we discuss potential therapeutic targets that may intercept this pathway and ultimately minimize long-term neurological decline.
      原文链接:
    • 万方数据

    Nanoparticles for the treatment of spinal cord injury

    Qiwei YangDi LuJiuping WuFuming Liang...
    1665-1680页
    查看更多>>摘要：Spinal cord injuries lead to significant loss of motor,sensory,and autonomic functions,presenting major challenges in neural regeneration.Achieving effective therapeutic concentrations at injury sites has been a slow process,partly due to the difficulty of delivering drugs effectively.Nanoparticles,with their targeted delivery capabilities,biocompatibility,and enhanced bioavailability over conventional drugs,are garnering attention for spinal cord injury treatment.This review explores the current mechanisms and shortcomings of existing treatments,highlighting the benefits and progress of nanoparticle-based approaches.We detail nanoparticle delivery methods for spinal cord injury,including local and intravenous injections,oral delivery,and biomaterial-assisted implantation,alongside strategies such as drug loading and surface modification.The discussion extends to how nanoparticles aid in reducing oxidative stress,dampening inflammation,fostering neural regeneration,and promoting angiogenesis.We summarize the use of various types of nanoparticles for treating spinal cord injuries,including metallic,polymeric,protein-based,inorganic non-metallic,and lipid nanoparticles.We also discuss the challenges faced,such as biosafety,effectiveness in humans,precise dosage control,standardization of production and characterization,immune responses,and targeted delivery in vivo.Additionally,we explore future directions,such as improving biosafety,standardizing manufacturing and characterization processes,and advancing human trials.Nanoparticles have shown considerable progress in targeted delivery and enhancing treatment efficacy for spinal cord injuries,presenting significant potential for clinical use and drug development.
      原文链接:
    • 万方数据
    • 维普