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{"title":"Chromatin accessibility regulates axon regeneration.","authors":"Isa Samad, Brett J Hilton","doi":"10.4103/NRR.NRR-D-24-01307","DOIUrl":"10.4103/NRR.NRR-D-24-01307","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1548-1549"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential targets of microglia in the treatment of neurodegenerative diseases: Mechanism and therapeutic implications.","authors":"Wenhui Zhao, Zhongxuan Liu, Jiannan Wu, Anran Liu, Junqiang Yan","doi":"10.4103/NRR.NRR-D-24-01343","DOIUrl":"10.4103/NRR.NRR-D-24-01343","url":null,"abstract":"<p><p>For diverse neurodegenerative disorders, microglial cells are activated. Furthermore, dysfunctional and hyperactivated microglia initiate mitochondrial autophagy, oxidative stress, and pathological protein accumulation, ending with neuroinflammation that exacerbates damage to dopaminergic neurons and contributes significantly to the pathology of neurodegenerative disorder. Microglial over-activation is closely associated with the secretion of pro-inflammatory cytokines, the phagocytosis of injured neurons, and the modulation of neurotoxic environments. This review summarizes the role of microglia neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, multiple system atrophy, amyotrophic lateral sclerosis, frontotemporal dementia, progressive supranuclear palsy, cortical degeneration, Lewy body dementia, and Huntington's disease. It also discusses novel forms of cell death such as ferroptosis, cuproptosis, disulfidptosis, and parthanatos (poly(adenosine diphosphate ribose) polymerase 1-dependent cell death), as well as the impact of regulatory factors related to microglial inflammation on microglial activation and neuroinflammation. The aim is to identify potential targets for microglial cell therapy in neurodegenerative diseases.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1497-1511"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenosine: A key player in neuroinflammation.","authors":"Qilin Guo, Rhea Seth, Wenhui Huang","doi":"10.4103/NRR.NRR-D-24-01486","DOIUrl":"10.4103/NRR.NRR-D-24-01486","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1556-1557"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular biomarkers in GNAO1 encephalopathies.","authors":"Vladimir L Katanaev, Jana Valnohova","doi":"10.4103/NRR.NRR-D-24-01550","DOIUrl":"10.4103/NRR.NRR-D-24-01550","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1570-1571"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Techniques and factors for reducing chronic neuropathic pain: A review.","authors":"Damien P Kuffler","doi":"10.4103/NRR.NRR-D-22-00015","DOIUrl":"10.4103/NRR.NRR-D-22-00015","url":null,"abstract":"<p><p>Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of pro-inflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of platelet-rich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1353-1358"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway.","authors":"Jie Jing, Shiling Chen, Xuan Wu, Jingfei Yang, Xia Liu, Jiahui Wang, Jingyi Wang, Yunjie Li, Ping Zhang, Zhouping Tang","doi":"10.4103/NRR.NRR-D-23-01953","DOIUrl":"10.4103/NRR.NRR-D-23-01953","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202604000-00038/figure1/v/2025-06-30T060627Z/r/image-tiff Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage. However, during minimally invasive surgery, recombinant tissue plasminogen activator may come into contact with brain tissue. Therefore, a thorough assessment of its safety is required. In this study, we established a mouse model of intracerebral hemorrhage induced by type VII collagenase. We observed that the administration of recombinant tissue plasminogen activator without hematoma aspiration significantly improved the neurological function of mice with intracerebral hemorrhage, reduced pathological damage, and lowered the levels of apoptosis and autophagy in the tissue surrounding the hematoma. In an in vitro model of intracerebral hemorrhage using primary cortical neurons induced by hemin, the administration of recombinant tissue plasminogen activator suppressed neuronal apoptosis, autophagy, and endoplasmic reticulum stress. Transcriptome sequencing analysis revealed that recombinant tissue plasminogen activator upregulated the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway in neurons. Moreover, the phosphoinositide 3-kinase inhibitor LY294002 abrogated the neuroprotective effects of recombinant tissue plasminogen activator in inhibiting excessive apoptosis, autophagy, and endoplasmic reticulum stress. Furthermore, to specify the domain of recombinant tissue plasminogen activator responsible for its neuroprotective effects, various inhibitors were used to target distinct domains. It has been revealed that the epidermal growth factor receptor inhibitor AG-1478 reversed the effect of recombinant tissue plasminogen activator on the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway. These findings suggest that recombinant tissue plasminogen activator exerts a direct neuroprotective effect on neurons following intracerebral hemorrhage, possibly through activation of the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1574-1585"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory T cells in neurological disorders and tissue regeneration: Mechanisms of action and therapeutic potentials.","authors":"Jing Jie, Xiaomin Yao, Hui Deng, Yuxiang Zhou, Xingyu Jiang, Xiu Dai, Yumin Yang, Pengxiang Yang","doi":"10.4103/NRR.NRR-D-24-01363","DOIUrl":"10.4103/NRR.NRR-D-24-01363","url":null,"abstract":"<p><p>Regulatory T cells, a subset of CD4 + T cells, play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties. Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair, emphasizing their multifaceted roles in immune regulation. This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration. Beyond their classical immune-regulatory functions, emerging evidence points to non-immune mechanisms of regulatory T cells, particularly their interactions with stem cells and other non-immune cells. These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration, positioning non-immune pathways as a promising direction for future research. By modulating immune and non-immune cells, including neurons and glia within neural tissues, Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems. Preclinical studies have revealed that Treg cells interact with neurons, glial cells, and other neural components to mitigate inflammatory damage and support functional recovery. Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment. However, research on the mechanistic roles of regulatory T cells in other diseases remains limited, highlighting substantial gaps and opportunities for exploration in this field. Laboratory and clinical studies have further advanced the application of regulatory T cells. Technical advances have enabled efficient isolation, ex vivo expansion and functionalization, and adoptive transfer of regulatory T cells, with efficacy validated in animal models. Innovative strategies, including gene editing, cell-free technologies, biomaterial-based recruitment, and in situ delivery have expanded the therapeutic potential of regulatory T cells. Gene editing enables precise functional optimization, while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites. These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair. By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair, regulatory T cells-based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1277-1291"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efferocytosis and retinal clean-up: Role of histone deacetylase 3 in ischemic retinopathy.","authors":"Abdelrahman Y Fouda, Esraa Shosha","doi":"10.4103/NRR.NRR-D-24-01342","DOIUrl":"10.4103/NRR.NRR-D-24-01342","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1572-1573"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum: Inhibiting SHP2 reduces glycolysis, promotes microglial M1 polarization, and alleviates secondary inflammation following spinal cord injury in a mouse model.","authors":"","doi":"10.4103/NRR.NRR-D-25-00703","DOIUrl":"10.4103/NRR.NRR-D-25-00703","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 4","pages":"1276"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of noninvasive brain stimulation on motor functions in animal models of ischemia and trauma in the central nervous system.","authors":"Seda Demir, Gereon R Fink, Maria A Rueger, Stefan J Blaschke","doi":"10.4103/NRR.NRR-D-24-01613","DOIUrl":"10.4103/NRR.NRR-D-24-01613","url":null,"abstract":"<p><p>Noninvasive brain stimulation techniques offer promising therapeutic and regenerative prospects in neurological diseases by modulating brain activity and improving cognitive and motor functions. Given the paucity of knowledge about the underlying modes of action and optimal treatment modalities, a thorough translational investigation of noninvasive brain stimulation in preclinical animal models is urgently needed. Thus, we reviewed the current literature on the mechanistic underpinnings of noninvasive brain stimulation in models of central nervous system impairment, with a particular emphasis on traumatic brain injury and stroke. Due to the lack of translational models in most noninvasive brain stimulation techniques proposed, we found this review to the most relevant techniques used in humans, i.e., transcranial magnetic stimulation and transcranial direct current stimulation. We searched the literature in PubMed, encompassing the MEDLINE and PMC databases, for studies published between January 1, 2020 and September 30, 2024. Thirty-five studies were eligible. Transcranial magnetic stimulation and transcranial direct current stimulation demonstrated distinct strengths in augmenting rehabilitation post-stroke and traumatic brain injury, with emerging mechanistic evidence. Overall, we identified neuronal, inflammatory, microvascular, and apoptotic pathways highlighted in the literature. This review also highlights a lack of translational surrogate parameters to bridge the gap between preclinical findings and their clinical translation.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1264-1276"},"PeriodicalIF":6.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}