全部最新文献

{"title":"Crucial role of microglia-mediated myelin sheath damage in vascular dementia: Antecedents and consequences.","authors":"Qi Shao, Simin Chen, Yuxiao Zheng, Wenxiu Xu, Jiahui Chen, Wei Shao, Qingguo Wang, Changxiang Li, Xueqian Wang","doi":"10.4103/NRR.NRR-D-24-01109","DOIUrl":"10.4103/NRR.NRR-D-24-01109","url":null,"abstract":"<p><p>Chronic cerebral hypoperfusion can lead to neuronal necrosis, trigger inflammatory responses, promote white matter damage, and ultimately result in cognitive impairment. Consequently, chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia. The myelin sheath is a critical component of white matter, and damage and repair of the white matter are closely linked to myelin sheath integrity. This article reviews the role of microglia in vascular dementia, focusing on their effects on myelin sheaths and the potential therapeutic implications. The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia, which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes. Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation. Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia. Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing, debris-clearing, and defensive mechanisms. However, prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype, resulting in myelin damage and cognitive impairment. Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia, as both are closely linked to cognitive decline. Although effective clinical treatments for myelin damage in the central nervous system are currently lacking, researchers are actively working to develop targeted therapies. Several drugs, including nimodipine, dopaminergic agents, simvastatin, biotin, and quetiapine, have been evaluated for clinical use in treating microglial and myelin damage. Future research will face challenges in developing targeted therapeutic strategies for vascular dementia, requiring further investigation into the timing, duration, and specific mechanisms of microglial activation, as well as the exploration of new drug combinations and additional therapeutic targets.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1000-1012"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720788","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":"Molecular mechanisms after optic nerve injury: Neurorepair strategies from a transcriptomic perspective.","authors":"Xiaxue Chen, Muyang Wei, Guangyu Li","doi":"10.4103/NRR.NRR-D-24-00794","DOIUrl":"10.4103/NRR.NRR-D-24-00794","url":null,"abstract":"<p><p>Retinal ganglion cells, a crucial component of the central nervous system, are often affected by irreversible visual impairment due to various conditions, including trauma, tumors, ischemia, and glaucoma. Studies have shown that the optic nerve crush model and glaucoma model are commonly used to study retinal ganglion cell injury. While these models differ in their mechanisms, both ultimately result in retinal ganglion cell injury. With advancements in high-throughput technologies, techniques such as microarray analysis, RNA sequencing, and single-cell RNA sequencing have been widely applied to characterize the transcriptomic profiles of retinal ganglion cell injury, revealing underlying molecular mechanisms. This review focuses on optic nerve crush and glaucoma models, elucidating the mechanisms of optic nerve injury and neuron degeneration induced by glaucoma through single-cell transcriptomics, transcriptome analysis, and chip analysis. Research using the optic nerve crush model has shown that different retinal ganglion cell subtypes exhibit varying survival and regenerative capacities following injury. Single-cell RNA sequencing has identified multiple genes associated with retinal ganglion cell protection and regeneration, such as Gal , Ucn , and Anxa2 . In glaucoma models, high-throughput sequencing has revealed transcriptomic changes in retinal ganglion cells under elevated intraocular pressure, identifying genes related to immune response, oxidative stress, and apoptosis. These genes are significantly upregulated early after optic nerve injury and may play key roles in neuroprotection and axon regeneration. Additionally, CRISPR-Cas9 screening and ATAC-seq analysis have identified key transcription factors that regulate retinal ganglion cell survival and axon regeneration, offering new potential targets for neurorepair strategies in glaucoma. In summary, single-cell transcriptomic technologies provide unprecedented insights into the molecular mechanisms underlying optic nerve injury, aiding in the identification of novel therapeutic targets. Future researchers should integrate advanced single-cell sequencing with multi-omics approaches to investigate cell-specific responses in retinal ganglion cell injury and regeneration. Furthermore, computational models and systems biology methods could help predict molecular pathways interactions, providing valuable guidance for clinical research on optic nerve regeneration and repair.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"989-999"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002704","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":"Efficacy of enhanced preoxygenation protocols in mitigating hypoxemia during propofol sedation for gastrointestinal endoscopic procedures: a prospective, randomized, controlled study.","authors":"Jun Lu, Wentao Ji, Yu Guo, Shun Yang, Didi Yang, Bo Li, Lulong Bo","doi":"10.4103/mgr.MEDGASRES-D-24-00136","DOIUrl":"10.4103/mgr.MEDGASRES-D-24-00136","url":null,"abstract":"<p><p>JOURNAL/mgres/04.03/01612956-202603000-00003/figure1/v/2025-06-28T140100Z/r/image-tiff Hypoxemia during propofol sedation for gastrointestinal endoscopic procedures is a significant risk and is often exacerbated by inadequate preoxygenation. Effective preoxygenation strategies are essential for reducing the incidence of hypoxemia, especially in high-risk patients. This study aimed to evaluate the efficacy of an enhanced preoxygenation protocol for mitigating hypoxemia during propofol sedation during gastroscopy. In a prospective, randomized, controlled design, patients undergoing gastroscopy were assigned to either an intervention group (enhanced preoxygenation) or a nonintervention group (standard care). The intervention protocol involved the administration of eight tidal volume breaths over 1 minute at an oxygen flow rate of 10 L/min via a tight-fitting face mask, with clinical supervision by an endoscopy nurse. The primary outcome was the incidence of hypoxemia, defined as a peripheral oxygen saturation level of less than 90% at any point during the gastroscopy procedure. Compared with the nonintervention group, the intervention group had a significantly lower incidence of hypoxemia. This effect was particularly pronounced in high-risk patients, including elderly individuals and those with elevated body mass indices. No significant adverse events were observed during the procedure. These results suggest that enhanced preoxygenation may effectively alleviate the occurrence of hypoxemia during propofol sedation in gastrointestinal endoscopic procedures. Further research is needed to assess the broader applicability of this approach and explore additional strategies for optimizing preoxygenation in endoscopic procedures.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"16 1","pages":"12-18"},"PeriodicalIF":3.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of central nervous system resident and recruited macrophages in the brain barrier system.","authors":"Ze Liu, Teng Cheng, Hongtian Dong, Dingya Sun, Yan Wang, Jiayan Li, Zhongwang Yu, Li Cao","doi":"10.4103/NRR.NRR-D-24-00986","DOIUrl":"10.4103/NRR.NRR-D-24-00986","url":null,"abstract":"<p><p>Macrophages in the brain barrier system include microglia in the brain parenchyma, border-associated macrophages at the brain's borders, and recruited macrophages. They are responsible for neural development, maintenance of homeostasis, and orchestrating immune responses. With the rapid exploitation and development of new technologies, there is a deeper understanding of macrophages in the brain barrier system. Here we review the origin, development, important molecules, and functions of macrophages, mainly focusing on microglia and border-associated macrophages. We also highlight some advances in single-cell sequencing and significant cell markers. We anticipate that more advanced methods will emerge to study resident and recruited macrophages in the future, opening new horizons for neuroimmunology and related peripheral immune fields.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"855-868"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066875","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":"Galectin 3: A new player in the pathogenesis of Parkinson's disease.","authors":"Juan García-Revilla, Jose Luis Venero, José A Rodríguez-Gómez","doi":"10.4103/NRR.NRR-D-24-01410","DOIUrl":"10.4103/NRR.NRR-D-24-01410","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1132-1133"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720905","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":"Traumatic brain injury: Bridging pathophysiological insights and precision treatment strategies.","authors":"Yujia Lu, Jie Jin, Huajing Zhang, Qianying Lu, Yingyi Zhang, Chuanchuan Liu, Yangfan Liang, Sijia Tian, Yanmei Zhao, Haojun Fan","doi":"10.4103/NRR.NRR-D-24-01398","DOIUrl":"10.4103/NRR.NRR-D-24-01398","url":null,"abstract":"<p><p>Blood-brain barrier disruption and the neuroinflammatory response are significant pathological features that critically influence disease progression and treatment outcomes. This review systematically analyzes the current understanding of the bidirectional relationship between blood-brain barrier disruption and neuroinflammation in traumatic brain injury, along with emerging combination therapeutic strategies. Literature review indicates that blood-brain barrier disruption and neuroinflammatory responses are key pathological features following traumatic brain injury. In the acute phase after traumatic brain injury, the pathological characteristics include primary blood-brain barrier disruption and the activation of inflammatory cascades. In the subacute phase, the pathological features are characterized by repair mechanisms and inflammatory modulation. In the chronic phase, the pathological features show persistent low-grade inflammation and incomplete recovery of the blood-brain barrier. Various physiological changes, such as structural alterations of the blood-brain barrier, inflammatory cascades, and extracellular matrix remodeling, interact with each other and are influenced by genetic, age, sex, and environmental factors. The dynamic balance between blood-brain barrier permeability and neuroinflammation is regulated by hormones, particularly sex hormones and stress-related hormones. Additionally, the role of gastrointestinal hormones is receiving increasing attention. Current treatment strategies for traumatic brain injury include various methods such as conventional drug combinations, multimodality neuromonitoring, hyperbaric oxygen therapy, and non-invasive brain stimulation. Artificial intelligence also shows potential in treatment decision-making and personalized therapy. Emerging sequential combination strategies and precision medicine approaches can help improve treatment outcomes; however, challenges remain, such as inadequate research on the mechanisms of the chronic phase traumatic brain injury and difficulties with technology integration. Future research on traumatic brain injury should focus on personalized treatment strategies, the standardization of techniques, cost-effectiveness evaluations, and addressing the needs of patients with comorbidities. A multidisciplinary approach should be used to enhance treatment and improve patient outcomes.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"887-907"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720764","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":"Hippocampal damage through foreign body placement in organotypic cultures leads to plastic responses in newly born granule cells.","authors":"Tassilo Jungenitz, Lukas Frey, Sophia Kirscht, Stephan W Schwarzacher, Angélica Zepeda","doi":"10.4103/NRR.NRR-D-24-00783","DOIUrl":"10.4103/NRR.NRR-D-24-00783","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00038/figure1/v/2025-06-16T082406Z/r/image-tiff The dentate gyrus of the hippocampus is a plastic structure that displays modifications at different levels in response to positive stimuli as well as to negative conditions such as brain damage. The latter involves global alterations, making understanding plastic responses triggered by local damage difficult. One key feature of the dentate gyrus is that it contains a well-defined neurogenic niche, the subgranular zone, and beyond neurogenesis, newly born granule cells may maintain a \"young\" phenotype throughout life, adding to the plastic nature of the structure. Here, we present a novel experimental model of local brain damage in organotypic entorhino-hippocampal cultures that results in the activation of adjacent newly born granule cells. A small piece of filter paper was placed on the surface of the granule cell layer of the dentate gyrus, which evoked a foreign body reaction of astrocytes, along with the activation of local young neurons expressing doublecortin. Forty-eight hours after foreign body placement, the number of doublecortin-immunoreactive cells increased in the subgranular zone in the direct vicinity of the foreign body, whereas overall increased doublecortin immunoreactivity was observed in the granule cell layer and molecular layer of the dentate gyrus. Foreign body placement in the pyramidal layer of the CA1 region evoked a comparable local astroglial reaction but did not lead to an increase in doublecortin-immunoreactive in either the CA1 region or the adjacent dentate gyrus. Seven days after foreign body placement in the dentate gyrus, the increase in doublecortin-immunoreactivity was no longer observed, indicating the transient activation of young cells. However, 7 days after foreign body placement, the number of doublecortin-immunoreactive granule cells coimmunoreactive for calbindin was lower than that under the control conditions. As calbindin is a marker for mature granule cells, this result suggests that activated young cells remain at a more immature stage following foreign body placement. Live imaging of retrovirally green fluorescent protein-labeled newly born granule cells revealed the orientation and growth of their dendrites toward the foreign body placement. This novel experimental model of foreign body placement in organotypic entorhino-hippocampal cultures could serve as a valuable tool for studying both glial reactivity and neuronal plasticity, specifically of newly born neurons under controlled in vitro conditions.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1142-1150"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813769","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":"Secretory autophagy in neurons: More than throwing out the trash?","authors":"Alexander Veh, Patrick Lüningschrör","doi":"10.4103/NRR.NRR-D-24-01514","DOIUrl":"10.4103/NRR.NRR-D-24-01514","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1108-1109"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720604","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":"Astrocyte glycolysis in Alzheimer's disease: When the stars burn out.","authors":"Simon M Bell, Heather Mortiboys","doi":"10.4103/NRR.NRR-D-24-01519","DOIUrl":"10.4103/NRR.NRR-D-24-01519","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1130-1131"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720851","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":"Astrocytes: Therapeutic targets for stroke.","authors":"Jingxiu Li, Keyuan Gao, Lili Wang, Jiayue Wang, Mian Qin, Xinrui Wang, Kai Lian, Chao Li, Shan'e Gao, Chenxi Sun","doi":"10.4103/NRR.NRR-D-24-01062","DOIUrl":"10.4103/NRR.NRR-D-24-01062","url":null,"abstract":"<p><p>Stroke is the leading cause of mortality globally, ultimately leading to severe, lifelong neurological impairments. Patients often suffer from a secondary cascade of damage, including neuroinflammation, cytotoxicity, oxidative stress, and mitochondrial dysfunction. Regrettably, there is a paucity of clinically available therapeutics to address these issues. Emerging evidence underscores the pivotal roles of astrocytes, the most abundant glial cells in the brain, throughout the various stages of ischemic stroke. In this comprehensive review, we initially provide an overview of the fundamental physiological functions of astrocytes in the brain, emphasizing their critical role in modulating neuronal homeostasis, synaptic activity, and blood-brain barrier integrity. We then delve into the growing body of evidence that highlights the functional diversity and heterogeneity of astrocytes in the context of ischemic stroke. Their well-established contributions to energy provision, metabolic regulation, and neurotransmitter homeostasis, as well as their emerging roles in mitochondrial recovery, neuroinflammation regulation, and oxidative stress modulation following ischemic injury, are discussed in detail. We also explore the cellular and molecular mechanisms underpinning these functions, with particular emphasis on recently identified targets within astrocytes that offer promising prospects for therapeutic intervention. In the final section of this review, we offer a detailed overview of the current therapeutic strategies targeting astrocytes in the treatment of ischemic stroke. These astrocyte-targeting strategies are categorized into traditional small-molecule drugs, microRNAs (miRNAs), stem cell-based therapies, cellular reprogramming, hydrogels, and extracellular vesicles. By summarizing the current understanding of astrocyte functions and therapeutic targeting approaches, we aim to highlight the critical roles of astrocytes during and after stroke, particularly in the pathophysiological development in ischemic stroke. We also emphasize promising avenues for novel, astrocyte-targeted therapeutics that could become clinically available options, ultimately improving outcomes for patients with stroke.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1074-1088"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780621","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}