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

    Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

    Yanxin ShenGuimei ZhangChunxiao WeiPanpan Zhao...
    613-631页
    查看更多>>摘要：Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis.Despite extensive research,a cure for Alzheimer's disease has not yet been found.Oxidative stress mediates excessive oxidative responses,and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted.As a member of the selenium-containing antioxidant enzyme family,glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis.With the discovery of ferroptosis,the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases,including Alzheimer's disease,has received widespread attention.Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain,resulting in oxidative stress,inflammation,ferroptosis,and apoptosis,which are closely associated with pathological damage in Alzheimer's disease.Several therapeutic approaches,such as small molecule drugs,natural plant products,and non-pharmacological treatments,ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity.Therefore,glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease.This review provides an overview of the gene structure,biological functions,and regulatory mechanisms of glutathione peroxidase 4,a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease,and a summary of the advances in small-molecule drugs,natural plant products,and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease.Most prior studies on this subject used animal models,and relevant clinical studies are lacking.Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.
      原文链接:
    • 万方数据

    Cell polarization in ischemic stroke:molecular mechanisms and advances

    Yuanwei LiXiaoxiao XuXuan WuJiarui Li...
    632-645页
    查看更多>>摘要：Ischemic stroke is a cerebrovascular disease associated with high mortality and disability rates.Since the inflammation and immune response play a central role in driving ischemic damage,it becomes essential to modulate excessive inflammatory reactions to promote cell survival and facilitate tissue repair around the injury site.Various cell types are involved in the inflammatory response,including microglia,astrocytes,and neutrophils,each exhibiting distinct phenotypic profiles upon stimulation.They display either proinflammatory or anti-inflammatory states,a phenomenon known as'cell polarization.'There are two cell polarization therapy strategies.The first involves inducing cells into a neuroprotective phenotype in vitro,then reintroducing them autologously.The second approach utilizes small molecular substances to directly affect cells in vivo.In this review,we elucidate the polarization dynamics of the three reactive cell populations(microglia,astrocytes,and neutrophils)in the context of ischemic stroke,and provide a comprehensive summary of the molecular mechanisms involved in their phenotypic switching.By unraveling the complexity of cell polarization,we hope to offer insights for future research on neuroinflammation and novel therapeutic strategies for ischemic stroke.
      原文链接:
    • 万方数据

    Toward understanding the role of genomic repeat elements in neurodegenerative diseases

    Zhengyu AnAidi JiangJingqi Chen
    646-659页
    查看更多>>摘要：Neurodegenerative diseases cause great medical and economic burdens for both patients and society;however,the complex molecular mechanisms thereof are not yet well understood.With the development of high-coverage sequencing technology,researchers have started to notice that genomic repeat regions,previously neglected in search of disease culprits,are active contributors to multiple neurodegenerative diseases.In this review,we describe the association between repeat element variants and multiple degenerative diseases through genome-wide association studies and targeted sequencing.We discuss the identification of disease-relevant repeat element variants,further powered by the advancement of long-read sequencing technologies and their related tools,and summarize recent findings in the molecular mechanisms of repeat element variants in brain degeneration,such as those causing transcriptional silencing or RNA-mediated gain of toxic function.Furthermore,we describe how in silico predictions using innovative computational models,such as deep learning language models,could enhance and accelerate our understanding of the functional impact of repeat element variants.Finally,we discuss future directions to advance current findings for a better understanding of neurodegenerative diseases and the clinical applications of genomic repeat elements.
      原文链接:
    • 万方数据
    • 维普

    From single to combinatorial therapies in spinal cord injuries for structural and functional restoration

    Ernesto Doncel-PérezGabriel Guízar-SahagúnIsrael Grijalva-Otero
    660-670页
    查看更多>>摘要：Spinal cord injury results in paralysis,sensory disturbances,sphincter dysfunction,and multiple systemic secondary conditions,most arising from autonomic dysregulation.All this produces profound negative psychosocial implications for affected people,their families,and their communities;the financial costs can be challenging for their families and health institutions.Treatments aimed at restoring the spinal cord after spinal cord injury,which have been tested in animal models or clinical trials,generally seek to counteract one or more of the secondary mechanisms of injury to limit the extent of the initial damage.Most published works on structural/functional restoration in acute and chronic spinal cord injury stages use a single type of treatment:a drug or trophic factor,transplant of a cell type,and implantation of a biomaterial.Despite the significant benefits reported in animal models,when translating these successful therapeutic strategies to humans,the result in clinical trials has been considered of little relevance because the improvement,when present,is usually insufficient.Until now,most studies designed to promote neuroprotection or regeneration at different stages after spinal cord injury have used single treatments.Considering the occurrence of various secondary mechanisms of injury in the acute and sub-acute phases of spinal cord injury,it is reasonable to speculate that more than one therapeutic agent could be required to promote structural and functional restoration of the damaged spinal cord.Treatments that combine several therapeutic agents,targeting different mechanisms of injury,which,when used as a single therapy,have shown some benefits,allow us to assume that they will have synergistic beneficial effects.Thus,this narrative review article aims to summarize current trends in the use of strategies that combine therapeutic agents administered simultaneously or sequentially,seeking structural and functional restoration of the injured spinal cord.
      原文链接:
    • 万方数据
    • 维普

    Crosstalk between degradation and bioenergetics:how autophagy and endolysosomal processes regulate energy production

    Angelid PabonJagannatham Naidu BhupanaChing-On Wong
    671-681页
    查看更多>>摘要：Cells undergo metabolic reprogramming to adapt to changes in nutrient availability,cellular activity,and transitions in cell states.The balance between glycolysis and mitochondrial respiration is crucial for energy production,and metabolic reprogramming stipulates a shift in such balance to optimize both bioenergetic efficiency and anabolic requirements.Failure in switching bioenergetic dependence can lead to maladaptation and pathogenesis.While cellular degradation is known to recycle precursor molecules for anabolism,its potential role in regulating energy production remains less explored.The bioenergetic switch between glycolysis and mitochondrial respiration involves transcription factors and organelle homeostasis,which are both regulated by the cellular degradation pathways.A growing body of studies has demonstrated that both stem cells and differentiated cells exhibit bioenergetic switch upon perturbations of autophagic activity or endolysosomal processes.Here,we highlighted the current understanding of the interplay between degradation processes,specifically autophagy and endolysosomes,transcription factors,endolysosomal signaling,and mitochondrial homeostasis in shaping cellular bioenergetics.This review aims to summarize the relationship between degradation processes and bioenergetics,providing a foundation for future research to unveil deeper mechanistic insights into bioenergetic regulation.
      原文链接:
    • 万方数据

    Corrigendum

    681页
      原文链接:
    • 万方数据
    • 维普

    Context-dependent role of sirtuin 2 in inflammation

    Noemí Sola-SevillaMaider Garmendia-BergesMCarmen Mera-DelgadoElena Puerta...
    682-694页
    查看更多>>摘要：Sirtuin 2 is a member of the sirtuin family nicotinamide adenine dinucleotide(NAD+)-dependent deacetylases,known for its regulatory role in different processes,including inflammation.In this context,sirtuin 2 has been involved in the modulation of key inflammatory signaling pathways and transcription factors by deacetylating specific targets,such as nuclear factor κB and nucleotide-binding oligomerization domain-leucine-rich-repeat and pyrin domain-containing protein 3(NLRP3).However,whether sirtuin 2-mediated pathways induce a pro-or an anti-inflammatory response remains controversial.Sirtuin 2 has been implicated in promoting inflammation in conditions such as asthma and neurodegenerative diseases,suggesting that its inhibition in these conditions could be a potential therapeutic strategy.Conversely,arthritis and type 2 diabetes mellitus studies suggest that sirtuin 2 is essential at the peripheral level and,thus,its inhibition in these pathologies would not be recommended.Overall,the precise role of sirtuin 2 in inflammation appears to be context-dependent,and further investigation is needed to determine the specific molecular mechanisms and downstream targets through which sirtuin 2 influences inflammatory processes in various tissues and pathological conditions.The present review explores the involvement of sirtuin 2 in the inflammation associated with different pathologies to elucidate whether its pharmacological modulation could serve as an effective strategy for treating this prevalent symptom across various diseases.
      原文链接:
    • 万方数据
    • 维普

    Liver as a new target organ in Alzheimer's disease:insight from cholesterol metabolism and its role in amyloid-beta clearance

    Beibei WuYuqing LiuHongli LiLemei Zhu...
    695-714页
    查看更多>>摘要：Alzheimer's disease,the primary cause of dementia,is characterized by neuropathologies,such as amyloid plaques,synaptic and neuronal degeneration,and neurofibrillary tangles.Although amyloid plaques are the primary characteristic of Alzheimer's disease in the central nervous system and peripheral organs,targeting amyloid-beta clearance in the central nervous system has shown limited clinical efficacy in Alzheimer's disease treatment.Metabolic abnormalities are commonly observed in patients with Alzheimer's disease.The liver is the primary peripheral organ involved in amyloid-beta metabolism,playing a crucial role in the pathophysiology of Alzheimer's disease.Notably,impaired cholesterol metabolism in the liver may exacerbate the development of Alzheimer's disease.In this review,we explore the underlying causes of Alzheimer's disease and elucidate the role of the liver in amyloid-beta clearance and cholesterol metabolism.Furthermore,we propose that restoring normal cholesterol metabolism in the liver could represent a promising therapeutic strategy for addressing Alzheimer's disease.
      原文链接:
    • 万方数据

    Targeting TrkB-PSD-95 coupling to mitigate neurological disorders

    Xin YangYu-Wen Alvin HuangJohn Marshall
    715-724页
    查看更多>>摘要：Tropomyosin receptor kinase B(TrkB)signaling plays a pivotal role in dendritic growth and dendritic spine formation to promote learning and memory.The activity-dependent release of brain-derived neurotrophic factor at synapses binds to pre-or postsynaptic TrkB resulting in the strengthening of synapses,reflected by long-term potentiation.Postsynaptically,the association of postsynaptic density protein-95 with TrkB enhances phospholipase Cy-Ca2+/calmodulin-dependent protein kinase Ⅱ and phosphatidylinositol 3-kinase-mechanistic target of rapamycin signaling required for long-term potentiation.In this review,we discuss TrkB-postsynaptic density protein-95 coupling as a promising strategy to magnify brain-derived neurotrophic factor signaling towards the development of novel therapeutics for specific neurological disorders.A reduction of TrkB signaling has been observed in neurodegenerative disorders,such as Alzheimer's disease and Huntington's disease,and enhancement of postsynaptic density protein-95 association with TrkB signaling could mitigate the observed deficiency of neuronal connectivity in schizophrenia and depression.Treatment with brain-derived neurotrophic factor is problematic,due to poor pharmacokinetics,low brain penetration,and side effects resulting from activation of the p75 neurotrophin receptor or the truncated TrkB.T1 isoform.Although TrkB agonists and antibodies that activate TrkB are being intensively investigated,they cannot distinguish the multiple human TrkB splicing isoforms or cell type-specific functions.Targeting TrkB-postsynaptic density protein-95 coupling provides an alternative approach to specifically boost TrkB signaling at localized synaptic sites versus global stimulation that risks many adverse side effects.
      原文链接:
    • 万方数据

    Spastin and alsin protein interactome analyses begin to reveal key canonical pathways and suggest novel druggable targets

    Benjamin R.HelmoldAngela AhrensZachary FitzgeraldP.Hande Ozdinler...
    725-739页
    查看更多>>摘要：Developing effective and long-term treatment strategies for rare and complex neurodegenerative diseases is challenging.One of the major roadblocks is the extensive heterogeneity among patients.This hinders understanding the underlying disease-causing mechanisms and building solutions that have implications for a broad spectrum of patients.One potential solution is to develop personalized medicine approaches based on strategies that target the most prevalent cellular events that are perturbed in patients.Especially in patients with a known genetic mutation,it may be possible to understand how these mutations contribute to problems that lead to neurodegeneration.Protein-protein interaction analyses offer great advantages for revealing how proteins interact,which cellular events are primarily involved in these interactions,and how they become affected when key genes are mutated in patients.This line of investigation also suggests novel druggable targets for patients with different mutations.Here,we focus on alsin and spastin,two proteins that are identified as"causative"for amyotrophic lateral sclerosis and hereditary spastic paraplegia,respectively,when mutated.Our review analyzes the protein interactome for alsin and spastin,the canonical pathways that are primarily important for each protein domain,as well as compounds that are either Food and Drug Administration-approved or are in active clinical trials concerning the affected cellular pathways.This line of research begins to pave the way for personalized medicine approaches that are desperately needed for rare neurodegenerative diseases that are complex and heterogeneous.
      原文链接:
    • 万方数据
    • 维普