Neural Regeneration Research最新文献

{"title":"Ultrashort wave therapy promotes traumatic brain injury recovery by suppressing neuroinflammation.","authors":"Chuang Xu, Jinwei Liu, Qiaozhen Qin, Heyang Zhang, Xiaotong Li, Yue Chen, Zhenhua Xu, Fang Wang, Nihui Zhang, Zhen Zhang, Yifei Tan, Lingyu Zhang, Guilin Chen, Liu Liu, Weiwei Xing, Yan Wang, Huaqiang Ruan, Xiaoxia Jiang, Nan Peng","doi":"10.4103/NRR.NRR-D-24-01479","DOIUrl":"10.4103/NRR.NRR-D-24-01479","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3609-3619"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982729","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":"Methods for a bioengineered 3D human brain-like tissue model of neuroregeneration after traumatic brain injury.","authors":"Marly Coe, Sydni Rosenfeld, Celia Byrne, Volha Liaudanskaya, David L Kaplan","doi":"10.4103/NRR.NRR-D-24-00497","DOIUrl":"10.4103/NRR.NRR-D-24-00497","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3620-3628"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020741","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":"Ferroptosis and aging: Inducing and catalyzing neurodegenerative diseases.","authors":"Qifeng Song, Shi Sun, Yuxiu Song, Yashi Wang, Yin Yuan, Lixin Zhang, Qian Cui","doi":"10.4103/NRR.NRR-D-25-00710","DOIUrl":"10.4103/NRR.NRR-D-25-00710","url":null,"abstract":"<p><p>Ferroptosis is a newly recognized form of programmed cell death characterized by iron overload-dependent lipid peroxidation. These pathological phenomena are often observed in neurodegenerative diseases. Aging is an irreversible process characterized by the deterioration of tissue and cell function. It has been shown to contribute to neurodegenerative diseases and increase susceptibility to ferroptosis. Therefore, ferroptosis may be involved in the progression of neurodegenerative diseases as a pathogenic factor, and aging is the common catalyst of both processes. The purpose of this review is to elucidate the latest progress on the mechanisms related to ferroptosis in neurodegenerative diseases, including iron overload, lipid peroxidation, antioxidant defense, cell membrane repair, and the regulation of autophagy and transcription factors. We also explored the relationship between ferroptosis and aging and reported that aging can induce ferroptosis by increasing iron overload, enhancing lipid peroxidation, and exacerbating autophagy disorders. Since ferroptosis is a pathogenic factor in neurodegenerative diseases, we screened gene bank databases and found that many genes associated with ferroptosis and neurodegenerative diseases overlap. Additionally, genes related to both the peroxidation pathway and ferroptosis are enriched. Ferroptosis occurs under conditions of age-related iron accumulation and lipid enrichment, as well as due to disorders in autophagy levels and transcription factors. Furthermore, in various neurodegenerative diseases, specific pathological changes or products can also contribute to the occurrence of ferroptosis. Finally, based on animal studies and clinical trials involving ferroptosis inhibitors, physical therapies, stem cell treatments, and exosome therapies in neurodegenerative diseases, it has been found that inhibiting ferroptosis can effectively reverse neurological dysfunction and cognitive impairment associated with these conditions. However, given various limitations, the conclusions of some animal studies and clinical trials have not been ideal, indicating that further large-scale research is necessary. Taken together, ferroptosis induces aging-related neurodegenerative diseases and neuronal cell death, triggering disease onset and progression. Ferroptosis inhibitors, physical therapies, stem cell treatments, and exosome therapies show great potential for inhibiting ferroptosis in neurodegenerative disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3462-3478"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993037","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":"MAPT -isoform 0N3R is essential for human brain development: Loss-of-function for novel TAU-associated disease paradigms.","authors":"Hans Zempel","doi":"10.4103/NRR.NRR-D-25-00298","DOIUrl":"10.4103/NRR.NRR-D-25-00298","url":null,"abstract":"<p><p>TAU, a microtubule-associated protein, encoded by the microtubule-associated protein tau ( MAPT ) gene, is a central regulator of microtubule stability and axonal function in the human brain, with its pathological aggregation representing a hallmark of Alzheimer's disease and related tauopathies. Despite extensive research into the role of TAU in neurodegeneration, its essentiality for human brain development has remained unclear. This perspective synthesizes recent genetic, molecular, and cellular evidence to demonstrate that the human brain-specific TAU isoform 0N3R is indispensable for proper neurodevelopment, pointing to loss-of-function of this isoform as a novel paradigm for TAU-associated disease. Alternative splicing of MAPT generates six brain-specific TAU isoforms, with 0N3R being exclusively expressed during fetal brain development. Analysis of large-scale human genetic datasets (gnomAD v4.0.0) reveals a high probability of loss-of-function intolerance (pLI = 0.96) for the 0N3R isoform. This is in stark contrast to the canonical Matched Annotation from the NCBI and EMBL-EBI (MANE) transcript and peripheral \"Big TAU,\" both of which are tolerant to loss-of-function mutations. This intolerance is further supported by the scarcity of loss-of-function mutations in 0N3R-encoding exons and high missense constraint scores, suggesting strong evolutionary selection against disruption of this isoform. Functional studies using human induced pluripotent stem cell-derived cortical neurons with CRISPR-Cas9-mediated MAPT knockout reveal that, unlike in murine models where compensation by other microtubule-associated proteins occurs, loss of TAU in human neurons leads to deficits in neurite outgrowth, axon initial segment shortening, and a trend toward hyperexcitability, accompanied by broad transcriptomic changes affecting genes involved in microtubule organization and synaptic structure. Remarkably, re-expression of any of the six human brain-specific TAU isoforms rescues these phenotypes, underscoring their functional redundancy during development. These findings position the 0N3R isoform as essential for human brain development and suggest that loss-of-function mutations affecting this isoform likely result in neurodevelopmental impairment, potentially manifesting as intellectual disability without overt dysmorphic features. This contrasts with the apparent tolerance to MAPT loss-of-function in mice and peripheral tissues, highlighting a critical species- and isoform-specific requirement for TAU in human neurodevelopment. The hypothesis of 0N3R-TAU loss-of-function intolerance opens new avenues for understanding neurodevelopmental disorders and refines the conceptual framework of TAU-associated disease mechanisms beyond toxic gain-of-function.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3349-3351"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186332","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":"Multimodal MRI combined with RNA sequencing reveals pathological signatures in the 9-month-old 3×Tg-AD mouse brain.","authors":"Yongxin Li, Ziling Tang, Maohua Yao, Yun Ran, Zuocheng Qiu","doi":"10.4103/NRR.NRR-D-25-00006","DOIUrl":"10.4103/NRR.NRR-D-25-00006","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3831-3841"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186382","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":"Gut microbial community of patients with Parkinson's disease analyzed using metagenome-assembled genomes.","authors":"Yi Zhang, Chengjun Mo, Xiaoqin He, Qin Xiao, Xiaodong Yang","doi":"10.4103/NRR.NRR-D-25-00420","DOIUrl":"10.4103/NRR.NRR-D-25-00420","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3815-3823"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186393","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":"Corrigendum: Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2.","authors":"","doi":"10.4103/NRR.NRRONLINE-D-26-00303","DOIUrl":"10.4103/NRR.NRRONLINE-D-26-00303","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 8","pages":"3386"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777341","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":"Gamma-type immunoglobulin enhances phagocytosis of amyloid-beta fibrils by microglia.","authors":"Tian Zhou, Yue Zhong, Shoujun Yu, Ruibing Sun, Zhenwei Zhang, Xiaoyan Du, Simon Ming-Yuen Lee, Zhitong Chen, Weiming Tian, Yuxiao Lai, Bing Song, Yiming Zheng, Zhen Xu","doi":"10.4103/NRR.NRR-D-23-01942","DOIUrl":"10.4103/NRR.NRR-D-23-01942","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3668-3676"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893906","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":"Enteric nervous system disease in neuronopathic lysosomal storage disorders.","authors":"Ewa A Ziółkowska, Robert O Heuckeroth, Jonathan D Cooper","doi":"10.4103/NRR.NRR-D-25-00448","DOIUrl":"10.4103/NRR.NRR-D-25-00448","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3537-3538"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859376","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":"TP53 drives neuronal ferroptosis by promoting KLHL4-mediated SLC7A11 ubiquitination after spinal cord injury.","authors":"Yu Kang, Qiangwei Li, Tianlun Zhao, Haojie Zhang, Yuejian Sun, Yilong Zhang, Da An, Zongsheng Yin, Yong Xuan, Peigen Xie","doi":"10.4103/NRR.NRR-D-24-01612","DOIUrl":"10.4103/NRR.NRR-D-24-01612","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"3717-3729"},"PeriodicalIF":6.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144992950","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}