医学最新文献

{"title":"Potential common pathogenesis of several neurodegenerative diseases.","authors":"Ting Fan, Jiaman Peng, Huiting Liang, Wenzhi Chen, Junlin Wang, Renshi Xu","doi":"10.4103/NRR.NRR-D-24-01054","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01054","url":null,"abstract":"<p><p>With the gradual advancement of research methods and technologies, various biological processes have been identified as playing roles in the pathogenesis of neurodegenerative diseases. However, current descriptions of these biological processes do not fully explain the onset, progression, and development of these conditions. Therefore, exploration of the pathogenesis of neurodegenerative diseases remains a valuable area of research. This review summarizes the potential common pathogeneses of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, frontotemporal lobar dementia, and Lewy body disease. Research findings have indicated that several common biological processes, including aging, genetic factors, progressive neuronal dysfunction, neuronal death and apoptosis, protein misfolding and aggregation, neuroinflammation, mitochondrial dysfunction, axonal transport defects, and gut microbiota dysbiosis, are involved in the pathogenesis of these six neurodegenerative diseases. Based on current information derived from diverse areas of research, these biological processes may form complex pathogenic networks that lead to distinctive types of neuronal death in neurodegenerative diseases. Furthermore, promoting the regeneration of damaged neurons may be achievable through the repair of affected neural cells if the underlying pathogenesis can be prevented or reversed. Hence, these potential common biological processes may represent only very small, limited elements within numerous intricate pathogenic networks associated with neurodegenerative diseases. In clinical treatment, interfering with any single biological process has proven insufficient to completely halt the progression of neurodegenerative diseases. Therefore, future research on the pathogenesis of neurodegenerative diseases should focus on uncovering the complex pathogenic networks, rather than isolating individual biological processes. Based on this, therapies that aim to block or reverse various targets involved in the potential pathogenic mechanisms of neurodegenerative diseases may be promising directions, as current treatment methods that focus on halting a single pathogenic factor have not achieved satisfactory efficacy.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"972-988"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310175","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":"Converging assemblies: A putative building block for brain function and for interfacing with the brain.","authors":"Eran Stark, Lidor Spivak","doi":"10.4103/NRR.NRR-D-24-01244","DOIUrl":"10.4103/NRR.NRR-D-24-01244","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1124-1125"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492995","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":"Short-chain fatty acids mediate enteric and central nervous system homeostasis in Parkinson's disease: Innovative therapies and their translation.","authors":"Shimin Pang, Zhili Ren, Hui Ding, Piu Chan","doi":"10.4103/NRR.NRR-D-24-01265","DOIUrl":"10.4103/NRR.NRR-D-24-01265","url":null,"abstract":"<p><p>Short-chain fatty acids, metabolites produced by the fermentation of dietary fiber by gut microbiota, have garnered significant attention due to their correlation with neurodegenerative diseases, particularly Parkinson's disease. In this review, we summarize the changes in short-chain fatty acid levels and the abundance of short-chain fatty acid-producing bacteria in various samples from patients with Parkinson's disease, highlighting the critical role of gut homeostasis imbalance in the pathogenesis and progression of the disease. Focusing on the nervous system, we discuss the molecular mechanisms by which short-chain fatty acids influence the homeostasis of both the enteric nervous system and the central nervous system. We identify key processes, including the activation of G protein-coupled receptors and the inhibition of histone deacetylases by short-chain fatty acids. Importantly, structural or functional disruptions in the enteric nervous system mediated by these fatty acids may lead to abnormal α-synuclein expression and gastrointestinal dysmotility, which could serve as an initiating event in Parkinson's disease. Furthermore, we propose that short-chain fatty acids help establish communication between the enteric nervous system and the central nervous system via the vagal nerve, immune circulation, and endocrine signaling. This communication may shed light on their potential role in the transmission of α-synuclein from the gut to the brain. Finally, we elucidate novel treatment strategies for Parkinson's disease that target short-chain fatty acids and examine the challenges associated with translating short-chain fatty acid-based therapies into clinical practice. In conclusion, this review emphasizes the pivotal role of short-chain fatty acids in regulating gut-brain axis integrity and their significance in the pathogenesis of Parkinson's disease from the perspective of the nervous system. Moreover, it highlights the potential value of short-chain fatty acids in early intervention for Parkinson's disease. Future research into the molecular mechanisms of short-chain fatty acids and their synergistic interactions with other gut metabolites is likely to advance the clinical translation of innovative short-chain fatty acid-based therapies for Parkinson's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"938-956"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143991184","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":"The engineered probiotic strain Lactococcus lactis MG1363-pMG36e-GLP-1 regulates microglial polarization and gut dysbiosis in a transgenic mouse model of Parkinson's disease.","authors":"Mengyun Yue, Tingtao Chen, Wenjie Chen, Jing Wei, Bin Liao, Jie Zhang, Fangjun Li, Daojun Hong, Xin Fang","doi":"10.4103/NRR.NRR-D-24-00702","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-00702","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00044/figure1/v/2025-06-16T082406Z/r/image-tiff Parkinson's disease is characterized by synucleinopathy-associated neurodegeneration. Previous studies have shown that glucagon-like peptide-1 (GLP-1) has beneficial effects in a mouse model of Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. However, the effect of GLP-1 on intrinsic synuclein malfunction remains unclear. In this study, we investigated the effect of Lactococcus lactis MG1363-pMG36e-GLP-1 on parkinsonism in SncaA53T transgenic mice and explored the underlying mechanisms. Our data showed that Lactococcus lactis MG1363-pMG36e-GLP-1 inhibited dopaminergic neuronal death, reduced pathological aggregation of α-synuclein, and decreased movement disorders in SncaA53T transgenic mice. Furthermore, Lactococcus lactis MG1363-pMG36e-GLP-1 downregulated lipopolysaccharide-related inflammation, reduced cerebral activation of microglia and astrocytes, and promoted cell survival via the GLP-1 receptor/PI3K/Akt pathway in the substantia nigra. Additionally, Lactococcus lactis MG1363-pMG36e-GLP-1 decreased serum levels of pro-inflammatory molecules including lipopolysaccharide, lipopolysaccharide binding protein, interleukin-1β, and interleukin-6. Gut histopathology and western blotting further revealed that Lactococcus lactis MG1363-pMG36e-GLP-1 increased the expression of gut integrity-related proteins and reduced lipopolysaccharide-related inflammation by reversing gut dysbiosis in SncaA53T transgenic mice. Our findings showed that the beneficial effect of Lactococcus lactis MG1363-pMG36e-GLP-1 on parkinsonism traits in SncaA53T transgenic mice is mediated by microglial polarization and the reversal of dysbiosis. Collectively, our findings suggest that Lactococcus lactis MG1363-pMG36e-GLP-1 is a promising therapeutic agent for the treatment of Parkinson's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"1211-1221"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310178","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":"Transplantation of human neural stem cells repairs neural circuits and restores neurological function in the stroke-injured brain.","authors":"Peipei Wang, Peng Liu, Yingying Ding, Guirong Zhang, Nan Wang, Xiaodong Sun, Mingyue Li, Mo Li, Xinjie Bao, Xiaowei Chen","doi":"10.4103/NRR.NRR-D-24-00363","DOIUrl":"10.4103/NRR.NRR-D-24-00363","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00040/figure1/v/2025-06-16T082406Z/r/image-tiff Exogenous neural stem cell transplantation has become one of the most promising treatment methods for chronic stroke. Recent studies have shown that most ischemia-reperfusion model rats recover spontaneously after injury, which limits the ability to observe long-term behavioral recovery. Here, we used a severe stroke rat model with 150 minutes of ischemia, which produced severe behavioral deficiencies that persisted at 12 weeks, to study the therapeutic effect of neural stem cells on neural restoration in chronic stroke. Our study showed that stroke model rats treated with human neural stem cells had long-term sustained recovery of motor function, reduced infarction volume, long-term human neural stem cell survival, and improved local inflammatory environment and angiogenesis. We also demonstrated that transplanted human neural stem cells differentiated into mature neurons in vivo , formed stable functional synaptic connections with host neurons, and exhibited the electrophysiological properties of functional mature neurons, indicating that they replaced the damaged host neurons. The findings showed that human fetal-derived neural stem cells had long-term effects for neurological recovery in a model of severe stroke, which suggests that human neural stem cells-based therapy may be effective for repairing damaged neural circuits in stroke patients.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1162-1171"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715856","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":"Spinal cord injury and inflammatory mediators: Role in \"fire barrier\" formation and potential for neural regeneration.","authors":"Mi Zhou, Zhengyu Xu, Hao Zhong, Guangzhi Ning, Shiqing Feng","doi":"10.4103/NRR.NRR-D-24-00792","DOIUrl":"10.4103/NRR.NRR-D-24-00792","url":null,"abstract":"<p><p>Traumatic spinal cord injury result in considerable and lasting functional impairments, triggering complex inflammatory and pathological events. Spinal cord scars, often metaphorically referred to as \"fire barriers,\" aim to control the spread of neuroinflammation during the acute phase but later hinder axon regeneration in later stages. Recent studies have enhanced our understanding of immunomodulation, revealing that injury-associated inflammation involves various cell types and molecules with positive and negative effects. This review employs bibliometric analysis to examine the literature on inflammatory mediators in spinal cord injury, highlighting recent research and providing a comprehensive overview of the current state of research and the latest advances in studies on neuroinflammation related to spinal cord injury. We summarize the immune and inflammatory responses at different stages of spinal cord injury, offering crucial insights for future research. Additionally, we review repair strategies based on inflammatory mediators for the injured spinal cord. Finally, this review discusses the current status and future directions of translational research focused on immune-targeting strategies, including pharmaceuticals, biomedical engineering, and gene therapy. The development of a combined, precise, and multitemporal strategy for the repair of injured spinal cords represents a promising direction for future research.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"923-937"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493022","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":"Role of the medullary reticular formation in motor control and functional recovery following spinal cord injury.","authors":"Frederic Bretzner","doi":"10.4103/NRR.NRR-D-24-01289","DOIUrl":"10.4103/NRR.NRR-D-24-01289","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1138-1139"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493020","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":"LncRNA regulation in ischemic stroke and their application prospects.","authors":"Qianqian Chen, Xiangyi Xu, Shun Li, Tianqing Xiong","doi":"10.4103/NRR.NRR-D-24-00924","DOIUrl":"10.4103/NRR.NRR-D-24-00924","url":null,"abstract":"<p><p>Ischemic stroke is a serious medical event that cannot be predicted in advance and can have long-lasting effects on patients, families, and communities. A deeper understanding of the changes in gene expression and the fundamental molecular mechanisms involved could help address this critical issue. In recent years, research into regulatory long non-coding (lnc)RNAs, a diverse group of RNA molecules with regulatory functions, has emerged as a promising direction in the study of cerebral infarction. This review paper aims to provide a comprehensive exploration of the roles of regulatory lncRNAs in cerebral infarction, as well as potential strategies for their application in clinical settings. LncRNAs have the potential to act as \"sponges\" that attract specific microRNAs, thereby regulating the expression of microRNA target genes. These interactions influence various aspects of ischemic stroke, including reperfusion-induced damage, cell death, immune responses, autophagy, angiogenesis, and the generation of reactive oxygen species. We highlight several regulatory lncRNAs that have been utilized in animal model treatments, including lncRNA NKILA, lncRNA Meg8, and lncRNA H19. Additionally, we discuss lncRNAs that have been used as biomarkers for the diagnosis and prognosis of cerebral infarction, such as lncRNA FOXO3, lncRNA XIST, and lncRNA RMST. The lncRNAs hold potential for genetic-level treatments in patients. However, numerous challenges, including inefficiency, low targeting accuracy, and side effects observed in preliminary studies, indicate the need for thorough investigation. The application of lncRNAs in ischemic stroke presents challenges that require careful and extensive validation.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1058-1073"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720910","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":"Potential and value of rescuing dying neurons.","authors":"Wenting You, Tos T J M Berendschot, Birke J Benedikter, Carroll A B Webers, Chris P M Reutelingsperger, Theo G M F Gorgels","doi":"10.4103/NRR.NRR-D-24-01134","DOIUrl":"10.4103/NRR.NRR-D-24-01134","url":null,"abstract":"<p><p>Unwarranted death of neurons is a major cause of neurodegenerative diseases. Since mature neurons are postmitotic and do not replicate, their death usually constitutes an irreversible step in pathology. A logical strategy to prevent neurodegeneration would then be to save all neurons that are still alive, i.e. protecting the ones that are still healthy as well as trying to rescue the ones that are damaged and in the process of dying. Regarding the latter, recent experiments have indicated that the possibility of reversing the cell death process and rescuing dying cells is more significant than previously anticipated. In many situations, the elimination of the cell death trigger alone enables dying cells to spontaneously repair their damage, recover, and survive. In this review, we explore the factors, which determine the fate of neurons engaged in the cell death process. A deeper insight into cell death mechanisms and the intrinsic capacity of cells to recover could pave the way for novel therapeutic approaches to neurodegenerative diseases.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1013-1022"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035631","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":"Preclinical safety and efficacy evaluation of the intrathecal transplantation of GMP-grade human umbilical cord mesenchymal stem cells for ischemic stroke.","authors":"Zejia Huang, Jiaohua Jiang, Qingxia Peng, Mengzhi Jin, Yakun Dong, Xuejia Li, Ermei Luo, Haijia Chen, Yidong Wang","doi":"10.4103/NRR.NRR-D-24-00683","DOIUrl":"10.4103/NRR.NRR-D-24-00683","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00041/figure1/v/2025-06-16T082406Z/r/image-tiff Intrathecal administration of human umbilical cord mesenchymal stem cells may be a promising approach for the treatment of stroke, but its safety, effectiveness, and mechanism remain to be elucidated. In this study, good manufacturing practice-grade human umbilical cord mesenchymal stem cells (5 × 10 5 and 1 × 10 6 cells) and saline were administered by cerebellomedullary cistern injection 72 hours after stroke induced by middle cerebral artery occlusion in rats. The results showed (1) no significant difference in mortality or general conditions among the three groups. There was no abnormal differentiation or tumor formation in various organs of rats in any group. (2) Compared with saline-treated animals, those treated with human umbilical cord mesenchymal stem cells showed significant functional recovery and reduced infarct volume, with no significant differences between different human umbilical cord mesenchymal stem cell doses. (3) Human umbilical cord mesenchymal stem cells were found in the ischemic brain after 14 and 28 days of follow-up, and the number of positive cells significantly decreased over time. (4) Neuronal nuclei expression in the human umbilical cord mesenchymal stem cell group was greater than that in the saline group, while glial fibrillary acidic protein and ionized calcium binding adaptor molecule 1 expression levels decreased. (5) Human umbilical cord mesenchymal stem cell treatment increased the number of CD31 + microvessels and doublecortin-positive cells after ischemic stroke. Human umbilical cord mesenchymal stem cells also upregulated the expression of CD31 + /Ki67 + . (6) At 14 days after intrathecal administration, brain-derived neurotrophic factor expression in the peri-infarct area and the concentrations of brain-derived neurotrophic factor in the cerebrospinal fluid in both human umbilical cord mesenchymal stem cell groups were significantly greater than those in the saline group and persisted until the 28 th day. Taken together, these results indicate that the intrathecal administration of human umbilical cord mesenchymal stem cells via cerebellomedullary cistern injection is safe and effective for the treatment of ischemic stroke in rats. The mechanisms may include alleviating the local inflammatory response in the peri-infarct region, promoting neurogenesis and angiogenesis, and enhancing the production of neurotrophic factors.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1172-1182"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716809","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}