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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

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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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    Mitophagy in acute central nervous system injuries:regulatory mechanisms and therapeutic potentials

    Siyi XuJunqiu JiaRui MaoXiang Cao...
    2437-2453页
    查看更多>>摘要:Acute central nervous system injuries,including ischemic stroke,intracerebral hemorrhage,subarachnoid hemorrhage,traumatic brain injury,and spinal cord injury,are a major global health challenge.Identifying optimal therapies and improving the long-term neurological functions of patients with acute central nervous system injuries are urgent priorities.Mitochondria are susceptible to damage after acute central nervous system injury,and this leads to the release of toxic levels of reactive oxygen species,which induce cell death.Mitophagy,a selective form of autophagy,is crucial in eliminating redundant or damaged mitochondria during these events.Recent evidence has highlighted the significant role of mitophagy in acute central nervous system injuries.In this review,we provide a comprehensive overview of the process,classification,and related mechanisms of mitophagy.We also highlight the recent developments in research into the role of mitophagy in various acute central nervous system injuries and drug therapies that regulate mitophagy.In the final section of this review,we emphasize the potential for treating these disorders by focusing on mitophagy and suggest future research paths in this area.

    Targeting harmful effects of non-excitatory amino acids as an alternative therapeutic strategy to reduce ischemic damage

    Victoria Jiménez CarreteroIris Álvarez-MerzJorge Hernández-CampanoSergei A.Kirov...
    2454-2463页
    查看更多>>摘要:The involvement of the excitatory amino acids glutamate and aspartate in cerebral ischemia and excitotoxicity is well-documented.Nevertheless,the role of non-excitatory amino acids in brain damage following a stroke or brain trauma remains largely understudied.The release of amino acids by necrotic cells in the ischemic core may contribute to the expansion of the penumbra.Our findings indicated that the reversible loss of field excitatory postsynaptic potentials caused by transient hypoxia became irreversible when exposed to a mixture of just four non-excitatory amino acids(L-alanine,glycine,L-glutamine,and L-serine)at their plasma concentrations.These amino acids induce swelling in the somas of neurons and astrocytes during hypoxia,along with permanent dendritic damage mediated by N-methyl-D-aspartate receptors.Blocking N-methyl-D-aspartate receptors prevented neuronal damage in the presence of these amino acids during hypoxia.It is likely that astroglial swelling caused by the accumulation of these amino acids via the alanine-serine-cysteine transporter 2 exchanger and system N transporters activates volume-regulated anion channels,leading to the release of excitotoxins and subsequent neuronal damage through N-methyl-D-aspartate receptor activation.Thus,previously unrecognized mechanisms involving non-excitatory amino acids may contribute to the progression and expansion of brain injury in neurological emergencies such as stroke and traumatic brain injury.Understanding these pathways could highlight new therapeutic targets to mitigate brain injury.

    Crosstalk among canonical Wnt and Hippo pathway members in skeletal muscle and at the neuromuscular junction

    Said HashemolhosseiniLea Gessler
    2464-2479页
    查看更多>>摘要:Skeletal muscles are essential for locomotion,posture,and metabolic regulation.To understand physiological processes,exercise adaptation,and muscle-related disorders,it is critical to understand the molecular pathways that underlie skeletal muscle function.The process of muscle contraction,orchestrated by a complex interplay of molecular events,is at the core of skeletal muscle function.Muscle contraction is initiated by an action potential and neuromuscular transmission requiring a neuromuscular junction.Within muscle fibers,calcium ions play a critical role in mediating the interaction between actin and myosin filaments that generate force.Regulation of calcium release from the sarcoplasmic reticulum plays a key role in excitation-contraction coupling.The development and growth of skeletal muscle are regulated by a network of molecular pathways collectively known as myogenesis.Myogenic regulators coordinate the differentiation of myoblasts into mature muscle fibers.Signaling pathways regulate muscle protein synthesis and hypertrophy in response to mechanical stimuli and nutrient availability.Several muscle-related diseases,including congenital myasthenic disorders,sarcopenia,muscular dystrophies,and metabolic myopathies,are underpinned by dysregulated molecular pathways in skeletal muscle.Therapeutic interventions aimed at preserving muscle mass and function,enhancing regeneration,and improving metabolic health hold promise by targeting specific molecular pathways.Other molecular signaling pathways in skeletal muscle include the canonical Wnt signaling pathway,a critical regulator of myogenesis,muscle regeneration,and metabolic function,and the Hippo signaling pathway.In recent years,more details have been uncovered about the role of these two pathways during myogenesis and in developing and adult skeletal muscle fibers,and at the neuromuscular junction.In fact,research in the last few years now suggests that these two signaling pathways are interconnected and that they jointly control physiological and pathophysiological processes in muscle fibers.In this review,we will summarize and discuss the data on these two pathways,focusing on their concerted action next to their contribution to skeletal muscle biology.However,an in-depth discussion of the non-canonical Wnt pathway,the fibro/adipogenic precursors,or the mechanosensory aspects of these pathways is not the focus of this review.

    Olfactory receptors in neural regeneration in the central nervous system

    Rafael FrancoClaudia GarrigósToni CapóJoan Serrano-Marín...
    2480-2494页
    查看更多>>摘要:Olfactory receptors are crucial for detecting odors and play a vital role in our sense of smell,influencing behaviors from food choices to emotional memories.These receptors also contribute to our perception of flavor and have potential applications in medical diagnostics and environmental monitoring.The ability of the olfactory system to regenerate its sensory neurons provides a unique model to study neural regeneration,a phenomenon largely absent in the central nervous system.Insights gained from how olfactory neurons continuously replace themselves and reestablish functional connections can provide strategies to promote similar regenerative processes in the central nervous system,where damage often results in permanent deficits.Understanding the molecular and cellular mechanisms underpinning olfactory neuron regeneration could pave the way for developing therapeutic approaches to treat spinal cord injuries and neurodegenerative diseases like Alzheimer's disease.Olfactory receptors are found in almost any cell of every organ/tissue of the mammalian body.This ectopic expression provides insights into the chemical structures that can activate olfactory receptors.In addition to odors,olfactory receptors in ectopic expression may respond to endogenous compounds and molecules produced by mucosal colonizing microbiota.The analysis of the function of olfactory receptors in ectopic expression provides valuable information on the signaling pathway engaged upon receptor activation and the receptor's role in proliferation and cell differentiation mechanisms.This review explores the ectopic expression of olfactory receptors and the role they may play in neural regeneration within the central nervous system,with particular attention to compounds that can activate these receptors to initiate regenerative processes.Evidence suggests that olfactory receptors could serve as potential therapeutic targets for enhancing neural repair and recovery following central nervous system injuries.

    The dopaminergic system and Alzheimer's disease

    Yuhan ZhangYuan LiangYixue Gu
    2495-2512页
    查看更多>>摘要:Alzheimer's disease is a common neurodegenerative disorder in older adults.Despite its prevalence,its pathogenesis remains unclear.In addition to the most widely accepted causes,which include excessive amyloid-beta aggregation,tau hyperphosphorylation,and deficiency of the neurotransmitter acetylcholine,numerous studies have shown that the dopaminergic system is also closely associated with the occurrence and development of this condition.Dopamine is a crucial catecholaminergic neurotransmitter in the human body.Dopamine-associated treatments,such as drugs that target dopamine receptor D and dopamine analogs,can improve cognitive function and alleviate psychiatric symptoms as well as ameliorate other clinical manifestations.However,therapeutics targeting the dopaminergic system are associated with various adverse reactions,such as addiction and exacerbation of cognitive impairment.This review summarizes the role of the dopaminergic system in the pathology of Alzheimer's disease,focusing on currently available dopamine-based therapies for this disorder and the common side effects associated with dopamine-related drugs.The aim of this review is to provide insights into the potential connections between the dopaminergic system and Alzheimer's disease,thus helping to clarify the mechanisms underlying the condition and exploring more effective therapeutic options.

    Acquired sensorineural hearing loss,oxidative stress,and microRNAs

    Desmond A.NunezRu C.Guo
    2513-2519页
    查看更多>>摘要:Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-factorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registered clinical trials known to the senior author were also assessed.A total of 222 studies were thus identified.After excluding duplicates,editorials,retractions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator-1-alpha(SIRT1/PGC-1α),SIRT1/p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adverse apoptotic effect,which was inhibited by resveratrol and a myocardial inhibitor-associated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

    Glucocorticoid receptor signaling in the brain and its involvement in cognitive function

    Chonglin SuTaiqi HuangMeiyu ZhangYanyu Zhang...
    2520-2537页
    查看更多>>摘要:The hypothalamic-pituitary-adrenal axis regulates the secretion of glucocorticoids in response to environmental challenges.In the brain,a nuclear receptor transcription factor,the glucocorticoid receptor,is an important component of the hypothalamic-pituitary-adrenal axis's negative feedback loop and plays a key role in regulating cognitive equilibrium and neuroplasticity.The glucocorticoid receptor influences cognitive processes,including glutamate neurotransmission,calcium signaling,and the activation of brain-derived neurotrophic factor-mediated pathways,through a combination of genomic and non-genomic mechanisms.Protein interactions within the central nervous system can alter the expression and activity of the glucocorticoid receptor,thereby affecting the hypothalamic-pituitary-adrenal axis and stress-related cognitive functions.An appropriate level of glucocorticoid receptor expression can improve cognitive function,while excessive glucocorticoid receptors or long-term exposure to glucocorticoids may lead to cognitive impairment.Patients with cognitive impairment-associated diseases,such as Alzheimer's disease,aging,depression,Parkinson's disease,Huntington's disease,stroke,and addiction,often present with dysregulation of the hypothalamic-pituitary-adrenal axis and glucocorticoid receptor expression.This review provides a comprehensive overview of the functions of the glucocorticoid receptor in the hypothalamic-pituitary-adrenal axis and cognitive activities.It emphasizes that appropriate glucocorticoid receptor signaling facilitates learning and memory,while its dysregulation can lead to cognitive impairment.This provides clues about how glucocorticoid receptor signaling can be targeted to overcome cognitive disability-related disorders.

    Nanocarrier-mediated siRNA delivery:a new approach for the treatment of traumatic brain injury-related Alzheimer's disease

    Jie JinHuajing ZhangQianying LuLinqiang Tian...
    2538-2555页
    查看更多>>摘要:Traumatic brain injury and Alzheimer's disease share pathological similarities,including neuronal loss,amyloid-β deposition,tau hyperphosphorylation,blood-brain barrier dysfunction,neuroinflammation,and cognitive deficits.Furthermore,traumatic brain injury can exacerbate Alzheimer's disease-like pathologies,potentially leading to the development of Alzheimer's disease.Nanocarriers offer a potential solution by facilitating the delivery of small interfering RNAs across the blood-brain barrier for the targeted silencing of key pathological genes implicated in traumatic brain injury and Alzheimer's disease.Unlike traditional approaches to neuroregeneration,this is a molecular-targeted strategy,thus avoiding non-specific drug actions.This review focuses on the use of nanocarrier systems for the efficient and precise delivery of siRNAs,discussing the advantages,challenges,and future directions.In principle,siRNAs have the potential to target all genes and non-targetable proteins,holding significant promise for treating various diseases.Among the various therapeutic approaches currently available for neurological diseases,siRNA gene silencing can precisely"turn off"the expression of any gene at the genetic level,thus radically inhibiting disease progression;however,a significant challenge lies in delivering siRNAs across the blood-brain barrier.Nanoparticles have received increasing attention as an innovative drug delivery tool for the treatment of brain diseases.They are considered a potential therapeutic strategy with the advantages of being able to cross the blood-brain barrier,targeted drug delivery,enhanced drug stability,and multifunctional therapy.The use of nanoparticles to deliver specific modified siRNAs to the injured brain is gradually being recognized as a feasible and effective approach.Although this strategy is still in the preclinical exploration stage,it is expected to achieve clinical translation in the future,creating a new field of molecular targeted therapy and precision medicine for the treatment of Alzheimer's disease associated with traumatic brain injury.

    Blood diagnostic and prognostic biomarkers in amyotrophic lateral sclerosis

    Yongting LvHongfu Li
    2556-2570页
    查看更多>>摘要:Amyotrophic lateral sclerosis is a devastating neurodegenerative disease for which the current treatment approaches remain severely limited.The principal pathological alterations of the disease include the selective degeneration of motor neurons in the brain,brainstem,and spinal cord,as well as abnormal protein deposition in the cytoplasm of neurons and glial cells.The biological markers under extensive scrutiny are predominantly located in the cerebrospinal fluid,blood,and even urine.Among these biomarkers,neurofilament proteins and glial fibrillary acidic protein most accurately reflect the pathologic changes in the central nervous system,while creatinine and creatine kinase mainly indicate pathological alterations in the peripheral nerves and muscles.Neurofilament light chain levels serve as an indicator of neuronal axonal injury that remain stable throughout disease progression and are a promising diagnostic and prognostic biomarker with high specificity and sensitivity.However,there are challenges in using neurofilament light chain to differentiate amyotrophic lateral sclerosis from other central nervous system diseases with axonal injury.Glial fibrillary acidic protein predominantly reflects the degree of neuronal demyelination and is linked to non-motor symptoms of amyotrophic lateral sclerosis such as cognitive impairment,oxygen saturation,and the glomerular filtration rate.TAR DNA-binding protein 43,a pathological protein associated with amyotrophic lateral sclerosis,is emerging as a promising biomarker,particularly with advancements in exosome-related research.Evidence is currently lacking for the value of creatinine and creatine kinase as diagnostic markers;however,they show potential in predicting disease prognosis.Despite the vigorous progress made in the identification of amyotrophic lateral sclerosis biomarkers in recent years,the quest for definitive diagnostic and prognostic biomarkers remains a formidable challenge.This review summarizes the latest research achievements concerning blood biomarkers in amyotrophic lateral sclerosis that can provide a more direct basis for the differential diagnosis and prognostic assessment of the disease beyond a reliance on clinical manifestations and electromyography findings.

    Spinal cord injury regenerative therapy development:integration of design of experiments

    Yuji OkanoHideyuki OkanoYoshitaka Kase
    2571-2573页