Neural Regeneration Research最新文献

{"title":"CD44-mediated meningeal monocyte activity enhances immune surveillance in the central nervous system after traumatic brain injury.","authors":"Qingxin Li, Mingyang Chai, Peikun Xu, Jiqing Hao","doi":"10.4103/NRR.NRR-D-24-01356","DOIUrl":"10.4103/NRR.NRR-D-24-01356","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5272-5283"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675521","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":"Organelles storing Ca 2+ in the brain cells: New druggable targets in neurodegenerative diseases.","authors":"Valentina Tedeschi, Raffaella Ciancio, Silvia Piccirillo, Alessandra Preziuso, Tiziano Serfilippi, Valentina Terenzi, Simona Magi, Vincenzo Lariccia, Pasqualina Castaldo, Antonio Vinciguerra, Ilaria Piccialli, Lorella Maria Teresa Canzoniero, Anna Pannaccione, Agnese Secondo","doi":"10.4103/NRR.NRR-D-25-01754","DOIUrl":"10.4103/NRR.NRR-D-25-01754","url":null,"abstract":"<p><p>Several lines of evidence suggest that targeting dysfunctional calcium (Ca 2+ )-storing organelles and their defective connections may represent a promising therapeutic strategy counteracting neurodegeneration. Dysfunction in these compartments converges to promote oxidative and endoplasmic reticulum stress, energy failure, autophagy blockade or hyperactivation, and progressive neurodegeneration. Within the intracellular scenario, several dysfunctional organelles have been characterized in terms of their capability to hijack Ca 2+ signaling during neurodegeneration to deadly impact on neuronal tasks in amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, brain ischemia, and neonatal hypoxic injury. This review has focused on the endoplasmic reticulum, mitochondria, and lysosomes, as well as their functional interconnection able to maintain the physiological processes such as lysosomal-dependent autophagy and function, lipid trafficking, and protein quality control. Clinically, looking ahead from the already existing therapies, drugs that enhance mitochondrial Ca 2+ efflux or modulate mitochondrial Ca 2+ uniporter regulation at mitochondria-associated membranes-endoplasmic reticulum sites represent innovative opportunities for next-generation strategies aimed at restoring mitochondrial homeostasis and protecting dopaminergic neurons in Parkinson's disease. Furthermore, functional stabilization of the lysosomal channel transient receptor potential mucolipin 1 by the lipid-based formulation of PI(3,5)P 2 may extend the lifespan of amyotrophic lateral sclerosis mice by stimulating the nuclear translocation of the master regulator of autophagy activated by lysosomal Ca 2+ release, namely transcription factor EB. Moreover, dysfunction of lysosomal-dependent autophagy can cause mutant huntingtin accumulation in Huntington's disease through the repression of transcription factor EB and lysophagy induction. Collectively, this growing focus may highlight a shift toward recognizing mitochondria, lysosomes, and endoplasmic reticulum, as well as their ionic machinery and interconnections, as a unifying strategy to maintain neuronal viability and mitigate the neurodegeneration progression in amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, lysosomal storage diseases, brain ischemia, and neonatal hypoxic insult.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5116-5125"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675112","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":"ALDH2 deficiency exacerbates acrolein-mediated neuropathology in multiple sclerosis.","authors":"Anna Alford, Siyuan Sun, Nathan Azimov, Zaiyang Zhang, Riyi Shi","doi":"10.4103/NRR.NRR-D-25-00825","DOIUrl":"10.4103/NRR.NRR-D-25-00825","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5641-5648"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148033491","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":"Retiring the sentinels: Could clearing senescent microglia be the answer to extending brain healthspan?","authors":"Rafaela Ferrão, Lino Ferreira, Vanessa Coelho-Santos","doi":"10.4103/NRR.NRR-D-25-01672","DOIUrl":"10.4103/NRR.NRR-D-25-01672","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5224-5225"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355858","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":"Aldehyde dehydrogenase-2 modulates acrolein toxicity to promote neural repair after spinal cord injury.","authors":"Siyuan Sun, Seth Herr, Anna Alford, Rachel Stingel, Zaiyang Zhang, Timothy Dong, Riyi Shi","doi":"10.4103/NRR.NRR-D-25-00833","DOIUrl":"10.4103/NRR.NRR-D-25-00833","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5304-5312"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675408","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":"An endogenous beta-endorphin corona confers neuroprotection against Alzheimer's amyloidogenesis.","authors":"Yunxiang Sun, Nicholas Andrikopoulos, Feng Ding, Pu Chun Ke","doi":"10.4103/NRR.NRR-D-25-01700","DOIUrl":"10.4103/NRR.NRR-D-25-01700","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5242-5243"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468961","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":"Piezo2 inhibition enhances the survival and axonal regeneration of spinal motoneurons after brachial plexus avulsion.","authors":"Yunsong Zhang, Fengwei Sun, Jin Wo, Lingtai Yu, Huandi Weng, Zhonghai Huang, Wen Li, Bin Jia, Meiting He, Ang Li, Libing Zhou","doi":"10.4103/NRR.NRR-D-25-00991","DOIUrl":"10.4103/NRR.NRR-D-25-00991","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5358-5368"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675113","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":"Identification of novel biomarkers for Alzheimer's disease: A deep learning omics-based approach to drug pair discovery and exploration of potential therapeutic targets.","authors":"Yuying Zhao, Jun Lei, Zixuan Wang, Siyuan Yang, Zhengduo Zhao, Yajun Xie, Jianhua Ran, Guangchao Zang","doi":"10.4103/NRR.NRR-D-25-00989","DOIUrl":"10.4103/NRR.NRR-D-25-00989","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5392-5403"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468346","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":"Dual strategies for neural injury repair: Targeted modulation of reactive astrocytes and functional astrocyte transplantation.","authors":"Zhenlu Cai, Xiang Zhou, Teng Teng, Hongli Li, Tunan Chen, Shuangshuang Dai, Kuan Zhang","doi":"10.4103/NRR.NRR-D-25-01020","DOIUrl":"10.4103/NRR.NRR-D-25-01020","url":null,"abstract":"<p><p>Reactive astrogliosis-the adaptive structural and functional remodeling responses of astrocytes-is a biphasic response to neural injury. While initially protective, it often transitions into a chronic, detrimental state characterized by sustained neuroinflammation, blood-brain barrier disruption, and excitotoxicity, which collectively impede recovery. To address this, this review systematically compares the responses of reactive astrocytes across three major neural pathologies-traumatic brain injury, ischemic stroke, and spinal cord injury-identifying both conserved molecular targets that are shared across injuries and stage-specific targets that are unique to distinct phases of injury. Moreover, this review proposes a dual-intervention paradigm that integrates timely pharmacological inhibition of detrimental reactive astrocyte activity with the transplantation of functional astrocytes, with the goal of restoring tissue homeostasis. Key issues elaborated upon include the profound heterogeneity of astrocyte responses, which complicates targeted therapy, and the translational barriers associated with cell transplantation. This review advocates for interventions focused on the regulation of astrocyte functions to adopt a dual intervention paradigm: specifically, timely pharmacological intervention to inhibit the abnormal activity of harmful reactive astrocytes, combined with the transplantation of functional astrocytes to replenish the beneficial cell populations needed for repair. The synergy of these two approaches aims to restore homeostasis in the tissue microenvironment. However, this requires further clarification of the phenotype transitions of reactive astrocytes at different pathological stages, as well as optimizing the timing of interventions and the efficiency of drug delivery to ensure the specificity and safety of the treatment, which is crucial for enhancing the effectiveness of the intervention.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5106-5115"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355743","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":"Ephrin and Eph family proteins: Molecular mechanisms of signaling pathways and their role in neural injury repair.","authors":"Xiaoyao Ma, Juan Liu, Qing Ma, Di Hu, Pengqin Wang, Shanli Yang, Mei Wang, Yurui Li, Hanqi Wang, Jiayi Liang, Yan Shao, Liang Zhang","doi":"10.4103/NRR.NRR-D-25-01845","DOIUrl":"10.4103/NRR.NRR-D-25-01845","url":null,"abstract":"<p><p>Ephrins and Eph family proteins are key intercellular signaling molecules in the nervous system. They regulate processes such as neural development, synaptic plasticity, neural stem cell differentiation, as well as neurodegenerative diseases and neural injury repair through a unique bidirectional signaling mechanism. In recent years, with the deepening of research, the central role of Ephrin and Eph family proteins in the field of neuroscience has gradually emerged, making them a hot topic of study. The purpose of this review is to systematically explore the mechanisms of action of Ephrin and Eph family proteins and their pathways in the nervous system, revealing their critical roles in neural development, functional maintenance, and disease occurrence, while providing theoretical foundations and potential targets for the treatment of neurological disorders. The Ephrin-Eph signaling pathway plays an important role in processes such as neuronal migration, axon guidance, synapse formation and plasticity, and neural stem cell differentiation through a bidirectional signaling mechanism. Abnormalities in this pathway are closely related to the development of neurodegenerative diseases (such as Alzheimer's disease), impairments in neural injury repair, and the progression of neurological tumors. Increasing evidence highlights the core regulatory position and functional complexity of Ephrin and Eph family proteins in the processes of neural injury and repair. The review also discusses the key regulatory roles of Ephrin and Eph family proteins in neuronal migration and positioning, axon guidance, synapse formation and plasticity, as well as their important functions in neural stem cell differentiation, cell adhesion and repulsion balance, and myelin regeneration. Additionally, this review analyzes the emerging roles of Ephrin and Eph family proteins in regulating the inflammatory microenvironment after neural injury, maintaining blood-brain barrier integrity, and facilitating neural function recovery. This review also summarizes the cellular and molecular mechanisms that support these functions, particularly the dynamic regulatory network of Ephrin-Eph bidirectional signaling and its interactions with other signaling pathways, such as Wnt and MAPK. Future research needs to further elucidate the molecular mechanisms of the Ephrin-Eph signaling pathway, develop highly specific small molecule inhibitors, gene therapy, and immunotherapy strategies, and integrate interdisciplinary technologies (such as single-cell multi-omics, optogenetics, and nanotechnology) to promote clinical translation, paving new avenues for precise treatment of neurological diseases.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5160-5170"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355734","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}