Neural Regeneration Research最新文献

{"title":"NLRP3 inflammasome and gut microbiota-brain axis: A new perspective on white matter injury after intracerebral hemorrhage.","authors":"Xiaoxi Cai, Xinhong Cai, Quanhua Xie, Xueqi Xiao, Tong Li, Tian Zhou, Haitao Sun","doi":"10.4103/NRR.NRR-D-24-00917","DOIUrl":"10.4103/NRR.NRR-D-24-00917","url":null,"abstract":"<p><p>Intracerebral hemorrhage is the most dangerous subtype of stroke, characterized by high mortality and morbidity rates, and frequently leads to significant secondary white matter injury. In recent decades, studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota-brain axis. This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury. The NACHT, LRR, and pyrin domain-containing protein 3 (NLRP3) inflammasome plays a crucial role in this context. This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome. These mechanisms include metabolic pathways (involving short-chain fatty acids, lipopolysaccharides, lactic acid, bile acids, trimethylamine-N-oxide, and tryptophan), neural pathways (such as the vagus nerve and sympathetic nerve), and immune pathways (involving microglia and T cells). We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage. The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood-brain barrier, inducing neuroinflammation, and interfering with nerve regeneration. Finally, we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury. Our review highlights the critical role of the gut microbiota-brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage, paving the way for exploring potential therapeutic approaches.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"62-80"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chitosan alleviates symptoms of Parkinson's disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood-brain barrier.","authors":"Yinying Wang, Rongsha Chen, Guolin Shi, Xinwei Huang, Ke Li, Ruohua Wang, Xia Cao, Zhongshan Yang, Ninghui Zhao, Jinyuan Yan","doi":"10.4103/NRR.NRR-D-23-01511","DOIUrl":"10.4103/NRR.NRR-D-23-01511","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202601000-00041/figure1/v/2025-06-09T151831Z/r/image-tiff Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse model of Parkinson's disease and found that it effectively reduced dopamine neuron injury, neurotransmitter dopamine release, and motor symptoms. These neuroprotective effects of chitosan were related to bacterial metabolites, specifically short-chain fatty acids, and chitosan administration altered intestinal microbial diversity and decreased short-chain fatty acid production in the gut. Furthermore, chitosan effectively reduced damage to the intestinal barrier and the blood-brain barrier. Finally, we demonstrated that chitosan improved intestinal barrier function and alleviated inflammation in both the peripheral nervous system and the central nervous system by reducing acetate levels. Based on these findings, we suggest a molecular mechanism by which chitosan decreases inflammation through reducing acetate levels and repairing the intestinal and blood-brain barriers, thereby alleviating symptoms of Parkinson's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"377-391"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141458356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglial polarization pathways and therapeutic drugs targeting activated microglia in traumatic brain injury.","authors":"Liping Shi, Shuyi Liu, Jialing Chen, Hong Wang, Zhengbo Wang","doi":"10.4103/NRR.NRR-D-24-00810","DOIUrl":"10.4103/NRR.NRR-D-24-00810","url":null,"abstract":"<p><p>Traumatic brain injury can be categorized into primary and secondary injuries. Secondary injuries are the main cause of disability following traumatic brain injury, which involves a complex multicellular cascade. Microglia play an important role in secondary injury and can be activated in response to traumatic brain injury. In this article, we review the origin and classification of microglia as well as the dynamic changes of microglia in traumatic brain injury. We also clarify the microglial polarization pathways and the therapeutic drugs targeting activated microglia. We found that regulating the signaling pathways involved in pro-inflammatory and anti-inflammatory microglia, such as the Toll-like receptor 4 /nuclear factor-kappa B, mitogen-activated protein kinase, Janus kinase/signal transducer and activator of transcription, phosphoinositide 3-kinase/protein kinase B, Notch, and high mobility group box 1 pathways, can alleviate the inflammatory response triggered by microglia in traumatic brain injury, thereby exerting neuroprotective effects. We also reviewed the strategies developed on the basis of these pathways, such as drug and cell replacement therapies. Drugs that modulate inflammatory factors, such as rosuvastatin, have been shown to promote the polarization of anti-inflammatory microglia and reduce the inflammatory response caused by traumatic brain injury. Mesenchymal stem cells possess anti-inflammatory properties, and clinical studies have confirmed their significant efficacy and safety in patients with traumatic brain injury. Additionally, advancements in mesenchymal stem cell-delivery methods-such as combinations of novel biomaterials, genetic engineering, and mesenchymal stem cell exosome therapy-have greatly enhanced the efficiency and therapeutic effects of mesenchymal stem cells in animal models. However, numerous challenges in the application of drug and mesenchymal stem cell treatment strategies remain to be addressed. In the future, new technologies, such as single-cell RNA sequencing and transcriptome analysis, can facilitate further experimental studies. Moreover, research involving non-human primates can help translate these treatment strategies to clinical practice.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"39-56"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential biofluid markers for cognitive impairment in Parkinson's disease.","authors":"Jieyu Chen, Chunyu Liang, Fang Wang, Yongyun Zhu, Liuhui Zhu, Jianzhun Chen, Bin Liu, Xinglong Yang","doi":"10.4103/NRR.NRR-D-24-00592","DOIUrl":"10.4103/NRR.NRR-D-24-00592","url":null,"abstract":"<p><p>Cognitive impairment is a particularly severe non-motor symptom of Parkinson's disease that significantly diminishes the quality of life of affected individuals. Identifying reliable biomarkers for cognitive impairment in Parkinson's disease is essential for early diagnosis, prognostic assessments, and the development of targeted therapies. This review aims to summarize recent advancements in biofluid biomarkers for cognitive impairment in Parkinson's disease, focusing on the detection of specific proteins, metabolites, and other biomarkers in blood, cerebrospinal fluid, and saliva. These biomarkers can shed light on the multifaceted etiology of cognitive impairment in Parkinson's disease, which includes protein misfolding, neurodegeneration, inflammation, and oxidative stress. The integration of biofluid biomarkers with neuroimaging and clinical data can facilitate the development of predictive models to enhance early diagnosis and monitor the progression of cognitive impairment in patients with Parkinson's disease. This comprehensive approach can improve the existing understanding of the mechanisms driving cognitive decline and support the development of targeted therapeutic strategies aimed at modifying the course of cognitive impairment in Parkinson's disease. Despite the promise of these biomarkers in characterizing the mechanisms underlying cognitive decline in Parkinson's disease, further research is necessary to validate their clinical utility and establish a standardized framework for early detection and monitoring of cognitive impairment in Parkinson's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"281-295"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared mechanisms and pathological phenotypes underlying aminoacyl-tRNA synthetase-related neuropathies.","authors":"Elena R Rhymes, James N Sleigh","doi":"10.4103/NRR.NRR-D-24-01080","DOIUrl":"10.4103/NRR.NRR-D-24-01080","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"312-313"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synaptic and synchronic impairments in subcortical brain regions associated with early non-cognitive dysfunction in Alzheimer's disease.","authors":"Nicolás Riffo-Lepe, Juliana González-Sanmiguel, Lorena Armijo-Weingart, Paulina Saavedra-Sieyes, David Hernandez, Gerson Ramos, Loreto S San Martín, Luis G Aguayo","doi":"10.4103/NRR.NRR-D-24-01052","DOIUrl":"10.4103/NRR.NRR-D-24-01052","url":null,"abstract":"<p><p>For many decades, Alzheimer's disease research has primarily focused on impairments within cortical and hippocampal regions, which are thought to be related to cognitive dysfunctions such as memory and language deficits. The exact cause of Alzheimer's disease is still under debate, making it challenging to establish an effective therapy or early diagnosis. It is widely accepted that the accumulation of amyloid-beta peptide in the brain parenchyma leads to synaptic dysfunction, a critical step in Alzheimer's disease development. The traditional amyloid cascade model is initiated by accumulating extracellular amyloid-beta in brain areas essential for memory and language. However, while it is possible to reduce the presence of amyloid-beta plaques in the brain with newer immunotherapies, cognitive symptoms do not necessarily improve. Interestingly, recent studies support the notion that early alterations in subcortical brain regions also contribute to brain damage and precognitive decline in Alzheimer's disease. A body of recent evidence suggests that early Alzheimer's disease is associated with alterations (e.g., motivation, anxiety, and motor impairment) in subcortical areas, such as the striatum and amygdala, in both human and animal models. Also, recent data indicate that intracellular amyloid-beta appears early in subcortical regions such as the nucleus accumbens, locus coeruleus, and raphe nucleus, even without extracellular amyloid plaques. The reported effects are mainly excitatory, increasing glutamatergic transmission and neuronal excitability. In agreement, data in Alzheimer's disease patients and animal models show an increase in neuronal synchronization that leads to electroencephalogram disturbances and epilepsy. The data indicate that early subcortical brain dysfunctions might be associated with non-cognitive symptoms such as anxiety, irritability, and motivation deficits, which precede memory loss and language alterations. Overall, the evidence reviewed suggests that subcortical brain regions could explain early dysfunctions and perhaps be targets for therapies to slow disease progression. Future research should focus on these non-traditional brain regions to reveal early pathological alterations and underlying mechanisms to advance our understanding of Alzheimer's disease beyond the traditionally studied hippocampal and cortical circuits.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"248-264"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adeno-associated viral vectors for modeling Parkinson's disease in non-human primates.","authors":"Julia Chocarro, José L Lanciego","doi":"10.4103/NRR.NRR-D-24-00896","DOIUrl":"10.4103/NRR.NRR-D-24-00896","url":null,"abstract":"<p><p>The development of clinical candidates that modify the natural progression of sporadic Parkinson's disease and related synucleinopathies is a praiseworthy endeavor, but extremely challenging. Therapeutic candidates that were successful in preclinical Parkinson's disease animal models have repeatedly failed when tested in clinical trials. While these failures have many possible explanations, it is perhaps time to recognize that the problem lies with the animal models rather than the putative candidate. In other words, the lack of adequate animal models of Parkinson's disease currently represents the main barrier to preclinical identification of potential disease-modifying therapies likely to succeed in clinical trials. However, this barrier may be overcome by the recent introduction of novel generations of viral vectors coding for different forms of alpha-synuclein species and related genes. Although still facing several limitations, these models have managed to mimic the known neuropathological hallmarks of Parkinson's disease with unprecedented accuracy, delineating a more optimistic scenario for the near future.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"224-232"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging role of microglia in the developing dopaminergic system: Perturbation by early life stress.","authors":"Kaijie She, Naijun Yuan, Minyi Huang, Wenjun Zhu, Manshi Tang, Qingyu Ma, Jiaxu Chen","doi":"10.4103/NRR.NRR-D-24-00742","DOIUrl":"10.4103/NRR.NRR-D-24-00742","url":null,"abstract":"<p><p>Early life stress correlates with a higher prevalence of neurological disorders, including autism, attention-deficit/hyperactivity disorder, schizophrenia, depression, and Parkinson's disease. These conditions, primarily involving abnormal development and damage of the dopaminergic system, pose significant public health challenges. Microglia, as the primary immune cells in the brain, are crucial in regulating neuronal circuit development and survival. From the embryonic stage to adulthood, microglia exhibit stage-specific gene expression profiles, transcriptome characteristics, and functional phenotypes, enhancing the susceptibility to early life stress. However, the role of microglia in mediating dopaminergic system disorders under early life stress conditions remains poorly understood. This review presents an up-to-date overview of preclinical studies elucidating the impact of early life stress on microglia, leading to dopaminergic system disorders, along with the underlying mechanisms and therapeutic potential for neurodegenerative and neurodevelopmental conditions. Impaired microglial activity damages dopaminergic neurons by diminishing neurotrophic support (e.g., insulin-like growth factor-1) and hinders dopaminergic axon growth through defective phagocytosis and synaptic pruning. Furthermore, blunted microglial immunoreactivity suppresses striatal dopaminergic circuit development and reduces neuronal transmission. Furthermore, inflammation and oxidative stress induced by activated microglia can directly damage dopaminergic neurons, inhibiting dopamine synthesis, reuptake, and receptor activity. Enhanced microglial phagocytosis inhibits dopamine axon extension. These long-lasting effects of microglial perturbations may be driven by early life stress-induced epigenetic reprogramming of microglia. Indirectly, early life stress may influence microglial function through various pathways, such as astrocytic activation, the hypothalamic-pituitary-adrenal axis, the gut-brain axis, and maternal immune signaling. Finally, various therapeutic strategies and molecular mechanisms for targeting microglia to restore the dopaminergic system were summarized and discussed. These strategies include classical antidepressants and antipsychotics, antibiotics and anti-inflammatory agents, and herbal-derived medicine. Further investigations combining pharmacological interventions and genetic strategies are essential to elucidate the causal role of microglial phenotypic and functional perturbations in the dopaminergic system disrupted by early life stress.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"126-140"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes in stroke management: A promising paradigm shift in stroke therapy.","authors":"Bo Wang, Pinzhen Chen, Wenyan Li, Zhi Chen","doi":"10.4103/NRR.NRR-D-24-00665","DOIUrl":"10.4103/NRR.NRR-D-24-00665","url":null,"abstract":"<p><p>Effective treatment methods for stroke, a common cerebrovascular disease with a high mortality rate, are still being sought. Exosome therapy, a form of acellular therapy, has demonstrated promising efficacy in various diseases in animal models; however, there is currently insufficient evidence to guide the clinical application of exosome in patients with stroke. This article reviews the progress of exosome applications in stroke treatment. It aims to elucidate the significant potential value of exosomes in stroke therapy and provide a reference for their clinical translation. At present, many studies on exosome-based therapies for stroke are actively underway. Regarding preclinical research, exosomes, as bioactive substances with diverse sources, currently favor stem cells as their origin. Due to their high plasticity, exosomes can be effectively modified through various physical, chemical, and genetic engineering methods to enhance their efficacy. In animal models of stroke, exosome therapy can reduce neuroinflammatory responses, alleviate oxidative stress damage, and inhibit programmed cell death. Additionally, exosomes can promote angiogenesis, repair and regenerate damaged white matter fiber bundles, and facilitate the migration and differentiation of neural stem cells, aiding the repair process. We also summarize new directions for the application of exosomes, specifically the exosome intervention through the ventricular-meningeal lymphatic system. The review findings suggest that the treatment paradigm for stroke is poised for transformation.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"6-22"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal plasticity and its role in Alzheimer's disease and Parkinson's disease.","authors":"Israt Jahan, Mohammad Harun-Ur-Rashid, Md Aminul Islam, Farhana Sharmin, Soad K Al Jaouni, Abdullah M Kaki, Samy Selim","doi":"10.4103/NRR.NRR-D-24-01019","DOIUrl":"10.4103/NRR.NRR-D-24-01019","url":null,"abstract":"<p><p>Neuronal plasticity, the brain's ability to adapt structurally and functionally, is essential for learning, memory, and recovery from injuries. In neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, this plasticity is disrupted, leading to cognitive and motor deficits. This review explores the mechanisms of neuronal plasticity and its effect on Alzheimer's disease and Parkinson's disease. Alzheimer's disease features amyloid-beta plaques and tau tangles that impair synaptic function, while Parkinson's disease involves the loss of dopaminergic neurons affecting motor control. Enhancing neuronal plasticity offers therapeutic potential for these diseases. A systematic literature review was conducted using databases such as PubMed, Scopus, and Google Scholar, focusing on studies of neuronal plasticity in Alzheimer's disease and Parkinson's disease. Data synthesis identified key themes such as synaptic mechanisms, neurogenesis, and therapeutic strategies, linking molecular insights to clinical applications. Results highlight that targeting synaptic plasticity mechanisms, such as long-term potentiation and long-term depression, shows promise. Neurotrophic factors, advanced imaging techniques, and molecular tools (e.g., clustered regularly interspaced short palindromic repeats and optogenetics) are crucial in understanding and enhancing plasticity. Current therapies, including dopamine replacement, deep brain stimulation, and lifestyle interventions, demonstrate the potential to alleviate symptoms and improve outcomes. In conclusion, enhancing neuronal plasticity through targeted therapies holds significant promise for treating neurodegenerative diseases. Future research should integrate multidisciplinary approaches to fully harness the therapeutic potential of neuronal plasticity in Alzheimer's disease and Parkinson's disease.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"107-125"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}