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{"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":"Sesquiterpene lactones as potential drugs treating nerve injury.","authors":"Philipp Gobrecht, Marco Leibinger, Dietmar Fischer","doi":"10.4103/NRR.NRR-D-24-00735","DOIUrl":"10.4103/NRR.NRR-D-24-00735","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 2","pages":"671-672"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029599","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":"Sox2-overexpressing neural stem cells alleviate ventricular enlargement and neurological dysfunction in posthemorrhagic hydrocephalus.","authors":"Baocheng Gao, Haoxiang Wang, Shuang Hu, Kunhong Zhong, Xiaoyin Liu, Ziang Deng, Yuanyou Li, Aiping Tong, Liangxue Zhou","doi":"10.4103/NRR.NRR-D-24-01491","DOIUrl":"10.4103/NRR.NRR-D-24-01491","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202602000-00045/figure1/v/2025-05-05T160104Z/r/image-tiff Neural stem cells (NSCs) have the potential for self-renewal and multidirectional differentiation, and their transplantation has achieved good efficacy in a variety of diseases. However, only 1%-10% of transplanted NSCs survive in the ischemic and hypoxic microenvironment of posthemorrhagic hydrocephalus. Sox2 is an important factor for NSCs to maintain proliferation. Therefore, Sox2-overexpressing NSCs (NSCSox2) may be more successful in improving neurological dysfunction after posthemorrhagic hydrocephalus. In this study, human NSCSox2 was transplanted into a posthemorrhagic hydrocephalus mouse model, and retinoic acid was administered to further promote NSC differentiation. The results showed that NSCSox2 attenuated the ventricular enlargement caused by posthemorrhagic hydrocephalus and improved neurological function. NSCSox2 also promoted nerve regeneration, inhibited neuroinflammation and promoted M2 polarization (anti-inflammatory phenotype), thereby reducing cerebrospinal fluid secretion in choroid plexus. These findings suggest that NSCSox2 rescued ventricular enlargement and neurological dysfunction induced by posthemorrhagic hydrocephalus through neural regeneration and modulation of inflammation.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 2","pages":"769-779"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037325","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":"Microglial intervention in ischemic stroke: Roles and intervention strategies.","authors":"Cuiling Ji, Lixinbei Sheng, Kaijun Han, Ping Yuan, Wei Li, Lu Chen, Yongyue Gao","doi":"10.4103/NRR.NRR-D-24-01166","DOIUrl":"10.4103/NRR.NRR-D-24-01166","url":null,"abstract":"<p><p>Ischemic stroke is a major cause of neurological deficits and high disability rate. As the primary immune cells of the central nervous system, microglia play dual roles in neuroinflammation and tissue repair following a stroke. Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes. This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies. Microglia exhibit a dynamic functional state, transitioning between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. This duality is crucial in ischemic stroke, as it maintains a balance between neuroinflammation and tissue repair. Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier, while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration. Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B, mitogen-activated protein kinases, Janus kinase/signal transducer and activator of transcription, and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways. These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage. Potential therapeutic agents include natural compounds found in drugs such as minocycline, as well as traditional Chinese medicines. Drugs that target these regulatory mechanisms, such as small molecule inhibitors and components of traditional Chinese medicines, along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics, offer new therapeutic strategies and clinical translational potential for ischemic stroke.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"443-454"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493015","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":"ABCA5 lipid transporter is associated with a reduced risk of Parkinson's disease.","authors":"Jasmin Galper, Nicolas Dzamko, Woojin Scott Kim","doi":"10.4103/NRR.NRR-D-24-01031","DOIUrl":"10.4103/NRR.NRR-D-24-01031","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"669-670"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008986","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":"Mitochondria-derived vesicles: New players in the game of neurodegeneration.","authors":"Laura Palumbo, Domenico Nuzzo, Antonella Girgenti, Pasquale Picone","doi":"10.4103/NRR.NRR-D-24-01220","DOIUrl":"10.4103/NRR.NRR-D-24-01220","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"679-680"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009009","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":"What is the pathophysiology of inflammation-induced cortical injury in the perinatal brain?","authors":"Sharmony B Kelly, Alistair J Gunn, Rodney W Hunt, Robert Galinsky","doi":"10.4103/NRR.NRR-D-24-01091","DOIUrl":"10.4103/NRR.NRR-D-24-01091","url":null,"abstract":"<p><p>Perinatal exposure to infection/inflammation is highly associated with neural injury, and subsequent impaired cortical growth, disturbances in neuronal connectivity, and impaired neurodevelopment. However, our understanding of the pathophysiological substrate underpinning these changes in brain structure and function is limited. The objective of this review is to summarize the growing evidence from animal trials and human cohort studies that suggest exposure to infection/inflammation during the perinatal period promotes regional impairments in neuronal maturation and function, including loss of high-frequency electroencephalographic activity, and reduced growth and arborization of cortical dendrites and dendritic spines resulting in reduced cortical volume. These inflammation-induced disturbances to neuronal structure and function are likely to underpin subsequent disturbances to cortical development and connectivity in fetuses and/or newborns exposed to infection/inflammation during the perinatal period, leading, in the long term, to impaired neurodevelopment. The combined use of early electroencephalography monitoring with neuroimaging techniques that enable detailed evaluation of brain microstructure, and the use of therapeutics that successfully target systemic and central nervous system inflammation could provide an effective strategy for early detection and therapeutic intervention.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"502-505"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066881","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}