Neural Regeneration Research最新文献

{"title":"Novel insights into non-coding RNAs and their role in hydrocephalus.","authors":"Zhiyue Cui, Jian He, An Li, Junqiang Wang, Yijian Yang, Kaiyue Wang, Zhikun Liu, Qian Ouyang, Zhangjie Su, Pingsheng Hu, Gelei Xiao","doi":"10.4103/NRR.NRR-D-24-00963","DOIUrl":"10.4103/NRR.NRR-D-24-00963","url":null,"abstract":"<p><p>A large body of evidence has highlighted the role of non-coding RNAs in neurodevelopment and neuroinflammation. This evidence has led to increasing speculation that non-coding RNAs may be involved in the pathophysiological mechanisms underlying hydrocephalus, one of the most common neurological conditions worldwide. In this review, we first outline the basic concepts and incidence of hydrocephalus along with the limitations of existing treatments for this condition. Then, we outline the definition, classification, and biological role of non-coding RNAs. Subsequently, we analyze the roles of non-coding RNAs in the formation of hydrocephalus in detail. Specifically, we have focused on the potential significance of non-coding RNAs in the pathophysiology of hydrocephalus, including glymphatic pathways, neuroinflammatory processes, and neurological dysplasia, on the basis of the existing evidence. Lastly, we review the potential of non-coding RNAs as biomarkers of hydrocephalus and for the creation of innovative treatments.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"636-647"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the transcriptomic heterogeneity of brain endothelial cells in normal aging and Alzheimer's disease.","authors":"Qian Yue, Shang Li, Chon Lok Lei, Huaibin Wan, Zaijun Zhang, Maggie Pui Man Hoi","doi":"10.4103/NRR.NRR-D-24-00695","DOIUrl":"10.4103/NRR.NRR-D-24-00695","url":null,"abstract":"<p><p>Drug development for Alzheimer's disease is extremely challenging, as demonstrated by the repeated failures of amyloid-β-targeted therapeutics and the controversies surrounding the amyloid-β cascade hypothesis. More recently, advances in the development of Lecanemab, an anti-amyloid-β monoclonal antibody, have shown positive results in reducing brain A burden and slowing cognitive decline in patients with early-stage Alzheimer's disease in the Phase III clinical trial (Clarity Alzheimer's disease). Despite these promising results, side effects such as amyloid-related imaging abnormalities (ARIA) may limit its usage. ARIA can manifest as ARIA-E (cerebral edema or effusions) and ARIA-H (microhemorrhages or superficial siderosis) and is thought to be caused by increased vascular permeability due to inflammatory responses, leading to leakages of blood products and protein-rich fluid into brain parenchyma. Endothelial dysfunction is an early pathological feature of Alzheimer's disease, and the blood-brain barrier becomes increasingly leaky as the disease progresses. In addition, APOE4, the strongest genetic risk factor for Alzheimer's disease, is associated with higher vascular amyloid burden, increased ARIA incidence, and accelerated blood-brain barrier disruptions. These interconnected vascular abnormalities highlight the importance of vascular contributions to the pathophysiology of Alzheimer's disease. Here, we will closely examine recent research evaluating the heterogeneity of brain endothelial cells in the microvasculature of different brain regions and their relationships with Alzheimer's disease progression.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"569-576"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mitophagy in spinal cord ischemia-reperfusion injury.","authors":"Yanni Duan, Fengguang Yang, Yibao Zhang, Mingtao Zhang, Yujun Shi, Yun Lang, Hongli Sun, Xin Wang, Hongyun Jin, Xuewen Kang","doi":"10.4103/NRR.NRR-D-24-00668","DOIUrl":"10.4103/NRR.NRR-D-24-00668","url":null,"abstract":"<p><p>Spinal cord ischemia-reperfusion injury, a severe form of spinal cord damage, can lead to sensory and motor dysfunction. This injury often occurs after traumatic events, spinal cord surgeries, or thoracoabdominal aortic surgeries. The unpredictable nature of this condition, combined with limited treatment options, poses a significant burden on patients, their families, and society. Spinal cord ischemia-reperfusion injury leads to reduced neuronal regenerative capacity and complex pathological processes. In contrast, mitophagy is crucial for degrading damaged mitochondria, thereby supporting neuronal metabolism and energy supply. However, while moderate mitophagy can be beneficial in the context of spinal cord ischemia-reperfusion injury, excessive mitophagy may be detrimental. Therefore, this review aims to investigate the potential mechanisms and regulators of mitophagy involved in the pathological processes of spinal cord ischemia-reperfusion injury. The goal is to provide a comprehensive understanding of recent advancements in mitophagy related to spinal cord ischemia-reperfusion injury and clarify its potential clinical applications.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"598-611"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A single-cell landscape of the regenerating spinal cord of zebrafish.","authors":"Lei Yao, Xinyi Cai, Saishuai Yang, Yixing Song, Lingyan Xing, Guicai Li, Zhiming Cui, Jiajia Chen","doi":"10.4103/NRR.NRR-D-24-01163","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01163","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202602000-00046/figure1/v/2025-05-05T160104Z/r/image-tiff Unlike mammals, zebrafish possess a remarkable ability to regenerate their spinal cord after injury, making them an ideal vertebrate model for studying regeneration. While previous research has identified key cell types involved in this process, the underlying molecular and cellular mechanisms remain largely unexplored. In this study, we used single-cell RNA sequencing to profile distinct cell populations at different stages of spinal cord injury in zebrafish. Our analysis revealed that multiple subpopulations of neurons showed persistent activation of genes associated with axonal regeneration post injury, while molecular signals promoting growth cone collapse were inhibited. Radial glial cells exhibited significant proliferation and differentiation potential post injury, indicating their intrinsic roles in promoting neurogenesis and axonal regeneration, respectively. Additionally, we found that inflammatory factors rapidly decreased in the early stages following spinal cord injury, creating a microenvironment permissive for tissue repair and regeneration. Furthermore, oligodendrocytes lost maturity markers while exhibiting increased proliferation following injury. These findings demonstrated that the rapid and orderly regulation of inflammation, as well as the efficient proliferation and redifferentiation of new neurons and glial cells, enabled zebrafish to reconstruct the spinal cord. This research provides new insights into the cellular transitions and molecular programs that drive spinal cord regeneration, offering promising avenues for future research and therapeutic strategies.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 2","pages":"780-789"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the role of ufmylation in the brain.","authors":"Rita J Serrano, Robert J Bryson-Richardson","doi":"10.4103/NRR.NRR-D-24-01311","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01311","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 2","pages":"667-668"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stress signaling caused by mitochondrial import malfunction can be terminated by SIFI: Importance of stress response silencing.","authors":"Grace Hohman, Michael Shahid, Mohamed A Eldeeb","doi":"10.4103/NRR.NRR-D-24-01169","DOIUrl":"10.4103/NRR.NRR-D-24-01169","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"673-674"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction.","authors":"Jun Wen, Hao Tang, Mingfen Tian, Ling Wang, Qinghuan Yang, Yong Zhao, Xuemei Li, Yu Ren, Jiani Wang, Li Zhou, Yongjun Tan, Haiyun Wu, Xinrui Cai, Yilin Wang, Hui Cao, Jianfeng Xu, Qin Yang","doi":"10.4103/NRR.NRR-D-24-00999","DOIUrl":"10.4103/NRR.NRR-D-24-00999","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202602000-00044/figure1/v/2025-05-05T160104Z/r/image-tiff Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment. However, little is known about how fibrosis is induced and regulated after cerebral ischemic injury. Sonic hedgehog signaling participates in fibrosis in the heart, liver, lung, and kidney. Whether Shh signaling modulates fibrotic scar formation after cerebral ischemic stroke and the underlying mechanisms are unclear. In this study, we found that Sonic Hedgehog expression was upregulated in patients with acute ischemic stroke and in a middle cerebral artery occlusion/reperfusion injury rat model. Both Sonic hedgehog and Mitofusin 2 showed increased expression in the middle cerebral artery occlusion rat model and in vitro fibrosis cell model induced by transforming growth factor-beta 1. Activation of the Sonic hedgehog signaling pathway enhanced the expression of phosphorylated Smad 3 and Mitofusin 2 proteins, promoted the formation of fibrotic scars, protected synapses or promoted synaptogenesis, alleviated neurological deficits following middle cerebral artery occlusion/reperfusion injury, reduced cell apoptosis, facilitated the transformation of meninges fibroblasts into myofibroblasts, and enhanced the proliferation and migration of meninges fibroblasts. The Smad3 phosphorylation inhibitor SIS3 reversed the effects induced by Sonic hedgehog signaling pathway activation. Bioinformatics analysis revealed significant correlations between Sonic hedgehog and Smad3, between Sonic hedgehog and Mitofusin 2, and between Smad3 and Mitofusin 2. These findings suggest that Sonic hedgehog signaling may influence Mitofusin 2 expression by regulating Smad3 phosphorylation, thereby modulating the formation of early fibrotic scars following cerebral ischemic stroke and affecting prognosis. The Sonic Hedgehog signaling pathway may serve as a new therapeutic target for stroke treatment.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"756-768"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intersection of mitochondrial dysfunction and myelination: An overlooked aspect in neurodevelopmental disorders.","authors":"Ariel Nir Sade, Gal Wiener, Boaz Barak","doi":"10.4103/NRR.NRR-D-24-01025","DOIUrl":"10.4103/NRR.NRR-D-24-01025","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"659-660"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural circuit mechanisms of epilepsy: Maintenance of homeostasis at the cellular, synaptic, and neurotransmitter levels.","authors":"Xueqing Du, Yi Wang, Xuefeng Wang, Xin Tian, Wei Jing","doi":"10.4103/NRR.NRR-D-24-00537","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-00537","url":null,"abstract":"<p><p>Epilepsy, a common neurological disorder, is characterized by recurrent seizures that can lead to cognitive, psychological, and neurobiological consequences. The pathogenesis of epilepsy involves neuronal dysfunction at the molecular, cellular, and neural circuit levels. Abnormal molecular signaling pathways or dysfunction of specific cell types can lead to epilepsy by disrupting the normal functioning of neural circuits. The continuous emergence of new technologies and the rapid advancement of existing ones have facilitated the discovery and comprehensive understanding of the neural circuit mechanisms underlying epilepsy. Therefore, this review aims to investigate the current understanding of the neural circuit mechanisms in epilepsy based on various technologies, including electroencephalography, magnetic resonance imaging, optogenetics, chemogenetics, deep brain stimulation, and brain-computer interfaces. Additionally, this review discusses these mechanisms from three perspectives: structural, synaptic, and transmitter circuits. The findings reveal that the neural circuit mechanisms of epilepsy encompass information transmission among different structures, interactions within the same structure, and the maintenance of homeostasis at the cellular, synaptic, and neurotransmitter levels. These findings offer new insights for investigating the pathophysiological mechanisms of epilepsy and enhancing its clinical diagnosis and treatment.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 2","pages":"455-465"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fat mass and obesity-mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury.","authors":"Xiangrong Chen, Jinqing Lai, Zhe Wu, Jianlong Chen, Baoya Yang, Chunnuan Chen, Chenyu Ding","doi":"10.4103/NRR.NRR-D-23-01854","DOIUrl":"10.4103/NRR.NRR-D-23-01854","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202602000-00042/figure1/v/2025-05-05T160104Z/r/image-tiff The neuroinflammatory response mediated by microglial activation plays an important role in the secondary nerve injury of traumatic brain injury. The post-transcriptional modification of N 6 -methyladenosine is ubiquitous in the immune response of the central nervous system. The fat mass and obesity-related protein catalyzes the demethylation of N 6 -methyladenosine modifications on mRNA and is widely expressed in various tissues, participating in the regulation of multiple diseases' biological processes. However, the role of fat mass and obesity in microglial activation and the subsequent neuroinflammatory response after traumatic brain injury is unclear. In this study, we found that the expression of fat mass and obesity was significantly down-regulated in both lipopolysaccharide-treated BV2 cells and a traumatic brain injury mouse model. After fat mass and obesity interference, BV2 cells exhibited a pro-inflammatory phenotype as shown by the increased proportion of CD11b + /CD86 + cells and the secretion of pro-inflammatory cytokines. Fat mass and obesity-mediated N 6 -methyladenosine demethylation accelerated the degradation of ADAM17 mRNA, while silencing of fat mass and obesity enhanced the stability of ADAM17 mRNA. Therefore, down-regulation of fat mass and obesity expression leads to the abnormally high expression of ADAM17 in microglia. These results indicate that the activation of microglia and neuroinflammatory response regulated by fat mass and obesity-related N 6 -methyladenosine modification plays an important role in the pro-inflammatory process of secondary injury following traumatic brain injury.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"730-741"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}