Neural Regeneration Research最新文献

{"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":"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}

{"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":"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":"Amyloid-β is NOT only the most promising target for Alzheimer's disease.","authors":"Beka Solomon, Milana Voronov-Goldman","doi":"10.4103/NRR.NRR-D-24-00829","DOIUrl":"10.4103/NRR.NRR-D-24-00829","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"681-682"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813719","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":"Recent advances in immunotherapy targeting amyloid-beta and tauopathies in Alzheimer's disease.","authors":"Sha Sha, Lina Ren, Xiaona Xing, Wanshu Guo, Yan Wang, Ying Li, Yunpeng Cao, Le Qu","doi":"10.4103/NRR.NRR-D-24-00846","DOIUrl":"10.4103/NRR.NRR-D-24-00846","url":null,"abstract":"<p><p>Alzheimer's disease, a devastating neurodegenerative disorder, is characterized by progressive cognitive decline, primarily due to amyloid-beta protein deposition and tau protein phosphorylation. Effectively reducing the cytotoxicity of amyloid-beta42 aggregates and tau oligomers may help slow the progression of Alzheimer's disease. Conventional drugs, such as donepezil, can only alleviate symptoms and are not able to prevent the underlying pathological processes or cognitive decline. Currently, active and passive immunotherapies targeting amyloid-beta and tau have shown some efficacy in mice with asymptomatic Alzheimer's disease and other transgenic animal models, attracting considerable attention. However, the clinical application of these immunotherapies demonstrated only limited efficacy before the discovery of lecanemab and donanemab. This review first discusses the advancements in the pathogenesis of Alzheimer's disease and active and passive immunotherapies targeting amyloid-beta and tau proteins. Furthermore, it reviews the advantages and disadvantages of various immunotherapies and considers their future prospects. Although some antibodies have shown promise in patients with mild Alzheimer's disease, substantial clinical data are still lacking to validate their effectiveness in individuals with moderate Alzheimer's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"577-587"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066873","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":"Metabolic reprogramming of astrocytes: Emerging roles of lactate.","authors":"Zeyu Liu, Yijian Guo, Ying Zhang, Yulei Gao, Bin Ning","doi":"10.4103/NRR.NRR-D-24-00776","DOIUrl":"10.4103/NRR.NRR-D-24-00776","url":null,"abstract":"<p><p>Lactate serves as a key energy metabolite in the central nervous system, facilitating essential brain functions, including energy supply, signaling, and epigenetic modulation. Moreover, it links epigenetic modifications with metabolic reprogramming. Nonetheless, the specific mechanisms and roles of this connection in astrocytes remain unclear. Therefore, this review aims to explore the role and specific mechanisms of lactate in the metabolic reprogramming of astrocytes in the central nervous system. The close relationship between epigenetic modifications and metabolic reprogramming was discussed. Therapeutic strategies for targeting metabolic reprogramming in astrocytes in the central nervous system were also outlined to guide future research in central nervous system diseases. In the nervous system, lactate plays an essential role. However, its mechanism of action as a bridge between metabolic reprogramming and epigenetic modifications in the nervous system requires future investigation. The involvement of lactate in epigenetic modifications is currently a hot research topic, especially in lactylation modification, a key determinant in this process. Lactate also indirectly regulates various epigenetic modifications, such as N6-methyladenosine, acetylation, ubiquitination, and phosphorylation modifications, which are closely linked to several neurological disorders. In addition, exploring the clinical applications and potential therapeutic strategies of lactic acid provides new insights for future neurological disease treatments.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"421-432"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838281","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":"Zebrafish optic nerve regeneration involves resident and retinal oligodendrocytes.","authors":"Cristina Pérez-Montes, Rosalía Hernández-García, Jhoana Paola Jiménez-Cubides, Laura DeOliveira-Mello, Almudena Velasco, Rosario Arévalo, Marina García-Macia, Adrián Santos-Ledo","doi":"10.4103/NRR.NRR-D-24-00621","DOIUrl":"10.4103/NRR.NRR-D-24-00621","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202602000-00049/figure1/v/2025-05-05T160104Z/r/image-tiff The visual system of teleost fish grows continuously, which is a useful model for studying regeneration of the central nervous system. Glial cells are key for this process, but their contribution is still not well defined. We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6, 24, and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy. To understand the changes that these oligodendrocytes undergo during regeneration, we used Sox2 immunohistochemistry, a stem cell marker involved in oligodendrocyte differentiation. We also used the Click-iT™ Plus TUNEL assay to study cell death and a BrdU assay to determine cell proliferation. Before optic nerve crush, sox10:tagRFP oligodendrocytes are located in the retina, in the optic nerve head, and through all the entire optic nerve. Sox2-positive cells are present in the peripheral germinal zone, the mature retina, and the optic nerve. After optic nerve crush, sox10:tagRFP cells disappeared from the optic nerve crush zone, suggesting that they died, although they were not TUNEL positive. Concomitantly, the number of Sox2-positive cells increased around the crushed area, the optic nerve head, and the retina. Then, between 24 hours post-lesion and 14 days post-lesion, double sox10:tagRFP /Sox2-positive cells were detected in the retina, optic nerve head, and whole optic nerve, together with a proliferation response at 72 hours post-lesion. Our results confirm that a degenerating process may occur prior to regeneration. First, sox10:tagRFP oligodendrocytes that surround the degenerated axons stop wrapping them, change their \"myelinating oligodendrocyte\" morphology to a \"nonmyelinating oligodendrocyte\" morphology, and die. Then, residual oligodendrocyte progenitor cells in the optic nerve and retina proliferate and differentiate for the purpose of remyelination. As new axons arise from the surviving retinal ganglion cells, new sox10:tagRFP oligodendrocytes arise from residual oligodendrocyte progenitor cells to guide, nourish and myelinate them. Thus, oligodendrocytes play an active role in zebrafish axon regeneration and remyelination.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"811-820"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059476","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":"Towards mechanism-based tau-targeted therapies.","authors":"Lidia Bakota, Roland Brandt","doi":"10.4103/NRR.NRR-D-24-01240","DOIUrl":"10.4103/NRR.NRR-D-24-01240","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"687-688"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009066","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":"Pathological axonal enlargement in connection with amyloidosis, lysosome destabilization, and bleeding is a major defect in Alzheimer's disease.","authors":"Hualin Fu, Jilong Li, Chunlei Zhang, Guo Gao, Qiqi Ge, Xinping Guan, Daxiang Cui","doi":"10.4103/NRR.NRR-D-24-01440","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01440","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202602000-00047/figure1/v/2025-05-05T160104Z/r/image-tiff Alzheimer's disease is a multi-amyloidosis disease characterized by amyloid-β deposits in brain blood vessels, microaneurysms, and senile plaques. How amyloid-β deposition affects axon pathology has not been examined extensively. We used immunohistochemistry and immunofluorescence staining to analyze the forebrain tissue slices of Alzheimer's disease patients. Widespread axonal amyloidosis with distinctive axonal enlargement was observed in patients with Alzheimer's disease. On average, amyloid-β-positive axon diameters in Alzheimer's disease brains were 1.72 times those of control brain axons. Furthermore, axonal amyloidosis was associated with microtubule-associated protein 2 reduction, tau phosphorylation, lysosome destabilization, and several blood-related markers, such as apolipoprotein E, alpha-hemoglobin, glycosylated hemoglobin type A1C, and hemin. Lysosome destabilization in Alzheimer's disease was also clearly identified in the neuronal soma, where it was associated with the co-expression of amyloid-β, Cathepsin D, alpha-hemoglobin, actin alpha 2, and collagen type IV. This suggests that exogenous hemorrhagic protein intake influences neural lysosome stability. Additionally, the data showed that amyloid-β-containing lysosomes were 2.23 times larger than control lysosomes. Furthermore, under rare conditions, axonal breakages were observed, which likely resulted in Wallerian degeneration. In summary, axonal enlargement associated with amyloidosis, micro-bleeding, and lysosome destabilization is a major defect in patients with Alzheimer's disease. This finding suggests that, in addition to the well-documented neural soma and synaptic damage, axonal damage is a key component of neuronal defects in Alzheimer's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 2","pages":"790-799"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025648","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}