Current Neuropharmacology最新文献

{"title":"Research Trends and Knowledge Atlas of Radiotherapy-Related Cognitive Impairment: A Bibliometric Analysis.","authors":"Yaqian Tan, Qi Song, Siyuan Gao","doi":"10.2174/011570159X368986250415105149","DOIUrl":"https://doi.org/10.2174/011570159X368986250415105149","url":null,"abstract":"<p><strong>Background: </strong>Radiotherapy is one of the main therapeutic methods for tumors, and radiation- related cognitive impairment has attracted increasing attention. The purpose of this study was to explore the research prospects in the field of radiotherapy-associated cognitive decline through bibliometric analysis.</p><p><strong>Methods: </strong>Literature on radiotherapy-related cognitive impairment published during 2004-2023 were extracted from the Web of Science Core Collection database. VOSviewer and R-bibliometrix were utilized to perform bibliometric analysis.</p><p><strong>Results: </strong>A total of 8,365 publications were retrieved from the database. The United States emerged as the leading country in this research field, with St. Jude Children's Research Hospital identified as the most productive institution. Thomas E. Merchant was the most prolific author in this field, while Charles L. Limoli was the most frequently cited scholar. The research hotspots have gradually shifted from cognitive function and outcome measurement to the development of new therapy models.</p><p><strong>Conclusion: </strong>This study comprehensively examined the research hotspots and knowledge atlas of radiotherapy- related cognitive decline from a bibliometric perspective. Our results would assist scholars in identifying potential collaborators and significant literature in this field while also providing valuable guidance for future research directions.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062628","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":"Excessive Urinary p75ecd is a Potential Indicator of Amyotrophic Lateral Sclerosis: An American Cohort Study.","authors":"Swati Dhasmana, Anupam Dhasmana, Sheema Khan, Acharan S Narula, Shafiul Haque, Murali M Yallapu, Subhash C Chauhan","doi":"10.2174/011570159X352364250212035802","DOIUrl":"https://doi.org/10.2174/011570159X352364250212035802","url":null,"abstract":"<p><strong>Introduction: </strong>Amyotrophic lateral sclerosis (ALS) is an idiopathic, fatal, and rapidly progressive neurodegenerative disease. At present, neurofilament light (NFL) and phosphorylated neurofilament heavy (pNfH) proteins in biological fluids are commonly known prognostic biomarkers, but their levels stabilize over time. Thus, there is a critical gap in the field to identify unique biomarkers that can aid disease diagnosis, progression and monitoring the therapy response.</p><p><strong>Aim: </strong>To evaluate the presence of extracellular domain of p75 (p75ecd) in urine of ALS patients and healthy control volunteers in the North American cohort.</p><p><strong>Method: </strong>An enzyme-linked immunoassay (ELISA) and creatinine assay was used to determine the levels of p75ecd and creatinine in the urine of ALS patients and healthy control volunteers respectively. This assay demonstrated clear discrimination in the levels of the p75ecd in the urine samples of ALS patients as compared to healthy individuals.</p><p><strong>Results: </strong>It was found that the concentration of p75ecd in ALS samples was significantly higher than that of healthy controls group. Additionally, high p75ecd levels were segregated with respect to age, sex, family history, occupation and drug treatment, medication status. Moreover, we observed differential expression patterns among the different stages of the disease. Our results followed the pattern that was observed in the Chinese, and Australian cohort.</p><p><strong>Conclusion: </strong>Altogether, our results indicate that the development of an efficient system for the detection of elevated levels of p75ecd in the urine could serve as a useful modality for early ALS diagnosis, disease progression, and monitoring the effectiveness of therapeutic interventions.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982659","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":"Hydroxychloroquine Prevents High-altitude Cerebral Edema by Inhibiting Endothelial Claudin-5 Autophagic Degradation.","authors":"Yan Xue, Baolan Wan, Zhen Wang, Zhiwei Wang, Dongzhi Wang, Wanping Yang, Xueting Wang, Li Zhu","doi":"10.2174/011570159X371235250417051313","DOIUrl":"10.2174/011570159X371235250417051313","url":null,"abstract":"<p><strong>Background: </strong>High-altitude cerebral edema (HACE) is a serious condition caused by pro-longed hypobaric hypoxia (HH). Autophagic degradation of Claudin-5 plays a crucial role in HH-induced blood-brain barrier (BBB) damage. Hydroxychloroquine (HCQ), a lysosomal inhibitor used in autophagy treatment, reduces inflammation and BBB damage in traumatic brain injury. However, its effectiveness in preventing HACE is still unknown.</p><p><strong>Methods: </strong>C57BL/6J mice were treated with HCQ and exposed to HH for 24 hrs to study BBB integ-rity. We evaluated BBB disruption via brain water content, Evans blue, and FITC-dextran assays. Changes in tight junctions (TJs) of cerebrovascular endothelial cells were analyzed using electron microscopy and immunofluorescence. Western blotting quantified autophagy protein levels in brain tissue. Hypoxia-mimetic in vitro models were used to explore HCQ's effects on TJs and BBB per-meability, confirmed by various assays, including immunofluorescence, electron microscopy, and Western blotting.</p><p><strong>Results: </strong>HCQ significantly mitigated rapamycin-induced autophagy and Claudin-5 degradation. Pro-longed hypoxia exposure promoted lysosomal degradation of Claudin-5, increasing endothelial cell permeability. HCQ inhibited autophagy in bEnd.3 cells via the PI3K-Akt-mTOR and Erk pathway, reducing hypoxia-induced Claudin-5 down-regulation. In mice, HH exposure increased brain au-tophagy, damaging the vascular endothelial TJs and subsequently increasing endothelial permeabil-ity. Pretreatment with HCQ significantly reduced the level of autophagy in the brains of HH-exposed mice, thereby mitigating the HH-induced damage to vascular TJs, alleviating the downregulation of Claudin-5, and enhancing endothelial integrity.</p><p><strong>Conclusion: </strong>HCQ effectively prevented HACE by inhibiting HH-induced Claudin-5 membrane ex-pression downregulation, thus mitigating BBB damage and brain water content increase in HH-exposed mice.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983905","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 Mechanisms and Application Prospects of Astrocyte Reprogramming into Neurons in Central Nervous System Diseases.","authors":"Rongxing Qin, Xinyu Lai, Wei Xu, Qingchun Qin, Xiaojun Liang, Minshan Xie, Li Chen","doi":"10.2174/011570159X379061250415094751","DOIUrl":"https://doi.org/10.2174/011570159X379061250415094751","url":null,"abstract":"<p><p>Central nervous system (CNS) diseases, including ischemic stroke (IS), Alzheimer's disease (AD), and Parkinson's disease (PD), are leading causes of global disability and mortality, characterized by progressive neuronal loss and irreversible neural circuit damage. Despite advances in understanding their pathophysiology, therapeutic options remain limited due to the complexity of disease mechanisms and challenges in delivering treatments across the blood-brain barrier (BBB). In this context, astrocyte reprogramming has emerged as a groundbreaking strategy for neural repair. By leveraging the plasticity of astrocytes, researchers have demonstrated the potential to convert these glial cells into functional neurons, offering a novel approach to replenish lost neurons and restore neural function. This review explores the latest advancements in astrocyte reprogramming, focusing on transcription factor-mediated, miRNA-induced, and small molecule-based strategies, as well as the molecular mechanisms underlying this process. We also discuss the therapeutic potential of astrocyte reprogramming in CNS diseases, including IS, AD, PD, and other neurodegenerative disorders, while addressing the challenges and future directions for clinical translation. Through a systematic analysis of recent studies, this review highlights the promise of astrocyte reprogramming as a transformative therapeutic strategy for CNS repair, providing new hope for patients with debilitating neurological conditions.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983168","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":"Vasoactive Intestinal Peptide: A Neuropeptide that Plays an Important Role in Parkinson's Disease.","authors":"Wenhui Fan, Ke Li, Ruohua Wang, Rongsha Chen, Yiben Liu, Zhongshan Yang, Ninghui Zhao, Jinyuan Yan","doi":"10.2174/011570159X374501250425045109","DOIUrl":"https://doi.org/10.2174/011570159X374501250425045109","url":null,"abstract":"<p><p>Parkinson's disease (PD) is primarily characterized by rigidity and tremor, which are pathologically associated with α -synuclein aggregation, especially in dopaminergic neurons in the midbrain. As it is a multi-factorial disease, there are currently no effective treatments but only mitigative therapies. Vasoactive intestinal peptide (VIP), a 28-amino acid neurotransmitter, is widely distributed in both the central and peripheral nervous system with a broad biological effect. Studies have shown that VIP exhibits anti-inflammatory, antioxidant, and anti-apoptotic effects and regulates glial cells and immune cells to protect and repair nerve cells. This article reviews the research progress of VIP as a brain-gut peptide in the treatment of PD and possible future research directions.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972965","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":"Nitric Oxide Metabolite Improves Cognitive Impairment by Reducing the Loss of Parvalbumin Inhibitory Interneurons in a Novel Mouse Model of Vascular Dementia.","authors":"Xiaorong Zhang, Lin Cheng, Seung-Bum Yang, Moon-Se Jin, Quanyu Piao, Dae-Weung Kim, Min-Sun Kim","doi":"10.2174/011570159X356939250306075324","DOIUrl":"https://doi.org/10.2174/011570159X356939250306075324","url":null,"abstract":"<p><strong>Background: </strong>This work aimed to develop a new and simple method to establish a mouse model of vascular dementia (VD). We investigated whether a new nitric oxide metabolite in the botanical mixture (a NO-donating botanical mixture, NOBM) improved learning and memory in mice that underwent bilateral carotid artery stenosis (BCAS).</p><p><strong>Method: </strong>C57BL/6N mice received the NOBM orally (0.1 mL twice a day) after BCAS, from days 1 to 28. We assessed spatial memory using the Y maze and place recognition tests at 1 week and 4 weeks after the induction of BCAS. We quantified the parvalbumin protein in the cortex and hippocampus at 1 week and 4 weeks. We also quantified expression levels of neuronal nuclei, brainderived neurotrophic factor, glial fibrillary acidic protein, and the number of dead neurons performed Fluoro-Jade B staining 31 days after BCAS.</p><p><strong>Results: </strong>NOBM significantly improved learning and memory behaviour in BCAS mice. Immunohistochemistry staining and Western blotting data showed a significantly higher protein expression of parvalbumin in the cortex and hippocampus of NOBM-treated BCAS animals, especially in the early stage of BCAS. Moreover, NOBM reduces neuronal loss in the cortex and reduces neuroinflammation and oxidative stress. The observed effect suggests that the NOBM reduced the loss of parvalbumin inhibitory interneurons in the early stage of VD and inhibited neuroinflammation in the VD mice model.</p><p><strong>Conclusion: </strong>Our results reveal a potential neuroprotective and therapeutic use of NOBM for cognitive dysfunction associated with cerebral hypoperfusion in a mouse model of VD.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977666","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":"Therapeutic Benefits of Bioactive Compounds in Brain Disorders.","authors":"Arianna Vignini","doi":"10.2174/011570159X404730250422071304","DOIUrl":"https://doi.org/10.2174/011570159X404730250422071304","url":null,"abstract":"","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972962","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 Extract of <i>Siegesbeckia orientalis</i> L. Reverses Pro-inflammatory Status of Microglia for Neuroprotection Following Ischemic Stroke in Mice.","authors":"Liu Bowen, Wan Bingjie, Zhao Xinyue, Zhao Yonghua, Yu Hua, Jiang Xuhong, Zheng Yanrong, Xu Yun","doi":"10.2174/011570159X349127241214045611","DOIUrl":"https://doi.org/10.2174/011570159X349127241214045611","url":null,"abstract":"<p><strong>Background: </strong><i>Siegesbeckia orientalis L. </i> (SO) is a traditional Chinese herbal medicine commonly used for inflammatory diseases. In ancient, SO is applied for stroke, but mechanisms have not been clear. The purpose is to investigate whether SO exerts neuroprotective effects by reducing microglia-related inflammatory injury after focal cerebral ischemia/reperfusion (I/R).</p><p><strong>Methods: </strong>SO was extracted using 50% ethanol and quality control was performed by Waters ACQUITY- UPLC CLASS system. The focal cerebral I/R model was established in mice, neurological functions, weight loss and infarct volume was evaluated. Microglial status in penumbra was monitored by immunofluorescence staining and morphology. Mouse primary microglia was subjected to lipopolysaccharide stimulation for triggering inflammatory response, meanwhile microglia-neuron co-culture model was established in vitro. Apoptosis and pyroptosis for neurons were demonstrated using TUNEL assay, western blot and ELISA. Inflammatory cytokines were detected by qPCR and ELISA.</p><p><strong>Results: </strong>SO treatment reduced infarct volume, improved neurological functions, lessened neuronal apoptosis and pyroptosis shown by increased Bcl-2/Bax ratio, decreased cleaved Caspase-3 and suppressed NLRP3/Caspase-1/GSDMD expression after I/R. Moreover, microglial status from proinflammation to anti-inflammation was characterized by morphological change and increasing percentage of CD206/Iba1 positive cells after SO treatment. Additionally, SO decreased TLR4 and nuclear- located p65 expression, suppressed IL-1β, IL-6, IL-18, and TNF-α, but increased IL-10 secretion both in vivo and vitro.</p><p><strong>Conclusion: </strong>SO reverses pro-inflammatory status of microglia as evidenced by suppression of TLR4/NF-κB cascade, down-regulation of pro-inflammatory cytokines and up-regulation of antiinflammatory cytokines, which contributes to its neuroprotective against neuronal pyroptosis and apoptosis after ischemic stroke.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989784","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":"Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.","authors":"Tong Shang, Binglin Kuang, Yaxin Shang, Wei Zou","doi":"10.2174/011570159X350639250403072430","DOIUrl":"https://doi.org/10.2174/011570159X350639250403072430","url":null,"abstract":"<p><p>Stroke is a leading cause of severe disability and mortality worldwide. Glial cells in the central nervous system (CNS) not only provide nutritional support but also play crucial roles in the inflammatory response. Microglia and astrocytes, integral components of the innate immune system, are involved in all stages of stroke and are active participants in inducing post-stroke neuroinflammation. Recent studies have increasingly focused on the potential crosstalk between microglia and astrocytes, identifying it as a promising area for understanding the pathogenesis and therapeutic mechanisms of CNS inflammatory diseases. These cells not only undergo dynamic phenotypic changes but also establish an intimate two-way dialogue by releasing various signaling molecules. This review paper elucidates the spatiotemporal dynamics of microglia and astrocytes in post-stroke neuroinflammation and highlights interaction pathways and potential therapeutic strategies for stroke.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989685","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 Prediction and Intervention of Internet Gaming Disorder.","authors":"Qinghua He, Hanlin Cheng","doi":"10.2174/011570159X390484250417063434","DOIUrl":"https://doi.org/10.2174/011570159X390484250417063434","url":null,"abstract":"","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989782","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}