Qian Zhao, Tiantian Liu, Jian Xing, Zixuan Kong, Dandan Hu, Miao Xia, Hongqiu Li, Zhenjun Chen, Lin Fei, Xinying Wang, Bin Liu, Feng Yang
{"title":"Exosome research and neuroimaging techniques: Visualization analysis of development trends and research hotspots.","authors":"Qian Zhao, Tiantian Liu, Jian Xing, Zixuan Kong, Dandan Hu, Miao Xia, Hongqiu Li, Zhenjun Chen, Lin Fei, Xinying Wang, Bin Liu, Feng Yang","doi":"10.4103/NRR.NRR-D-26-00586","DOIUrl":"10.4103/NRR.NRR-D-26-00586","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5485-5496"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795914","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":"Amyotrophic lateral sclerosis: Neural repair strategies based on multi-target synchronous interventions.","authors":"Jingjing Liu, Lijun Zhou, Youqing Deng, Renshi Xu","doi":"10.4103/NRR.NRR-D-25-00221","DOIUrl":"10.4103/NRR.NRR-D-25-00221","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis is a progressive and fatal neurodegenerative disease that targets motor neurons in the cerebral cortex, medulla oblongata, and spinal cord. This review focuses on the current concepts in the aetiopathogenesis and diagnosis of amyotrophic lateral sclerosis, aiming to explore potential neural repair strategies (curative and/or progression-retarding therapeutics). Recent studies have highlighted that the complex pathogenesis of amyotrophic lateral sclerosis is related to its multifactorial aetiology, including proteostasis disruption, impaired RNA metabolism and DNA repair, cytoskeletal and axonal transport defects, excitotoxicity, neuroinflammation, mitochondrial dysfunction, oligodendrocyte dysfunction, nucleocytoplasmic transport deficits, lipid dyshomeostasis, and autophagy. Several approved drugs are currently used to treat patients with amyotrophic lateral sclerosis; however, their curative efficacy is limited. Thus, the search for effective therapeutic strategies for amyotrophic lateral sclerosis requires a comprehensive understanding of its pathogenesis. Current evidence indicates that a single drug cannot provide a satisfactory therapeutic effect. Additionally, multiple pathophysiological processes and related targets are involved in the pathogenesis of amyotrophic lateral sclerosis. Therefore, research on multi-target synchronous interventions may be the path forward for discovering and developing potential neural repair strategies.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5181-5195"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100379","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":"Potassium-dependent coupling of retinal astrocytes and Müller glia.","authors":"Joseph M Holden, David J Calkins","doi":"10.4103/NRR.NRR-D-25-01563","DOIUrl":"10.4103/NRR.NRR-D-25-01563","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5220-5221"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355868","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":"Analysis of the dual role of amyloid-beta in Alzheimer's disease through multi-omics integration.","authors":"Jingwen Guo, Xiaoqin Lu, Luying Qiu, Weishuang Xue, Hefei Fu, Keke Wang, Yanzhe Wang","doi":"10.4103/NRR.NRR-D-25-00872","DOIUrl":"10.4103/NRR.NRR-D-25-00872","url":null,"abstract":"<p><p>Accumulation of amyloid-beta is highly important in the development of Alzheimer's disease. Given the limitations of the amyloid cascade hypothesis and the repeated clinical failures of anti-amyloid-beta therapies, researchers are increasingly exploring the infection hypothesis. This review explores the dual behaviors of amyloid-beta in Alzheimer's disease, with a particular focus on its protective role against infection by microorganisms and its complicated connections with innate immune system. This new opinion holds that amyloid-beta can play an antimicrobial peptide role. During microbial invasion, its original role is to protect neural tissue, but prolonged accumulation leads to chronic deposition and involvement in pathological processes. Evidence from in vitro experiments, animal models, and clinical studies indicates that amyloid-beta may possess antiviral and antibacterial properties, particularly against infections such as herpes simplex virus, human immunodeficiency virus, and Porphyromonas gingivalis . However, excessive accumulation of amyloid beta triggers a neuroinflammatory cascade that impairs neuronal regeneration and cognitive function. Despite substantial research into Alzheimer's disease, current treatments have not yielded significant clinical benefits. Although monoclonal antibodies such as Aducanumab , Lecanemab , and Donanemab have been approved for marketing, their strict indications and high costs pose challenges for widespread promotion. The infection hypothesis of amyloid-beta has spurred clinical trials investigating vaccines targeting specific pathogens to assess their potential in preventing or treating Alzheimer's disease. This highlights the need for further exploring the multifaceted role of amyloid-beta in Alzheimer's disease. In addition, microbial infections can also trigger or regulate genetic and epigenetic factors, accelerating amyloid beta deposition. Among them, the apolipoprotein E epsilon 4 allele is the strongest genetic risk factor for Alzheimer's disease, as it exacerbates the accumulation of amyloid beta and promotes neuroinflammation. Strategies targeting epigenetic regulation may provide novel approaches to inhibit Alzheimer's disease pathology. This review also integrates various technologies such as genomics, proteomics, and metabolomics. This provides a broader system-level understanding of the risk gene loci, protein interaction networks, and metabolic changes associated with amyloid beta under the influence of microbial infections. Such techniques may lead to the identification of new molecular targets, the development of individualized treatment strategies, and the creation of early biomarkers for use in clinical research. In conclusion, this review suggests that amyloid-beta is not merely a pathological by-product but an environmentally responsive molecule with dual functions. A deeper understanding of the dynamic regulation of amyloid-beta, considering infection status and disease s","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5171-5180"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100348","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":"Blood-retinal biomarker integration for precision prevention of Alzheimer's disease: Lessons from retinal aging and the unfolded protein response.","authors":"Monica L Acosta, Sarah X Zhang, Adrian G Palacios","doi":"10.4103/NRR.NRR-D-25-01517","DOIUrl":"10.4103/NRR.NRR-D-25-01517","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5230-5231"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355770","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}
Shiyuan Chen, Jingjing Li, Jianwen Zhou, Wenyuan Xie, Huidong Li, Li Yang, Gong Chen, Cheng Long
{"title":"NeuroD1 gene therapy converts reactive astrocytes to functional new neurons in a mouse model of Alzheimer's disease.","authors":"Shiyuan Chen, Jingjing Li, Jianwen Zhou, Wenyuan Xie, Huidong Li, Li Yang, Gong Chen, Cheng Long","doi":"10.4103/NRR.NRR-D-25-00721","DOIUrl":"10.4103/NRR.NRR-D-25-00721","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"5604-5612"},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147674905","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}