Current Neuropharmacology最新文献

{"title":"A Novel Network Pharmacology Strategy for Retrieving a Key Functional Component Group and Mechanisms in the Di-Huang-Yin-Zi Treatment of Parkinson's Disease.","authors":"Qi Qu, Yanfei Tong, Yi Li, Han Zhang, Jianhua Yang, Zongwei Cai, Siqiang Ren, Daogang Guan, Shaogang Qu","doi":"10.2174/011570159X378077250822115218","DOIUrl":"https://doi.org/10.2174/011570159X378077250822115218","url":null,"abstract":"<p><strong>Introduction: </strong>Parkinson's Disease (PD) is a common and difficult-to-cure chronic neurodegenerative disorder. Current medications often target a single pathway and can have certain side effects. In contrast, traditional Chinese medicine formulas, such as Di-Huang-Yin-Zi (DHYZ), with their multi-component and multi-target characteristics, offer potential advantages by addressing these limitations, making them worthy of in-depth study.</p><p><strong>Methods: </strong>Components of DHYZ were collected from public databases and literature. After screening, the remaining components underwent target prediction, and the predicted component-target pairs were used to construct the complex component-target network. A novel node importance algorithm, known as the fusion model, was applied to construct an effective space from the component-target network, thereby reducing redundancy. Meanwhile, the pathological genes were extracted from DisGeNET and GeneCards to judge the quality of effective space. The effective space was compared with other widely used network parameters to validate its efficiency, and the Key Functional Compound Group (KFCG) was inferred from the effective space. Finally, the protective mechanism of DHYZ was inferred based on the KFCG and was validated in the in vitro PD model.</p><p><strong>Results: </strong>Compared to other commonly used algorithms, the effective space identified by the fusion model more accurately represented the full spectrum of DHYZ's targets and demonstrated stronger correlation with PD. Additionally, we utilized the component contribution ratio algorithm to identify the KFCG within the effective space. Through enrichment analysis, we hypothesized that KFCG may exert its anti-PD effects via the PI3K-Akt, MAPK, and AMPK pathways and validated these mechanisms in vitro.</p><p><strong>Discussion: </strong>Collectively, the results of this study not only deepen our understanding of the therapeutic potential of DHYZ in the treatment of PD but also enhance the clinical translatability of DHYZ through formula optimization. However, this study has certain limitations. For instance, the pathogenic genes of PD were not incorporated into the network in this study, and the use of an undirected network may offer lower biological interpretability compared to a directed network.</p><p><strong>Conclusion: </strong>This robust and precise algorithm allowed us to optimize Di-Huang-Yin-Zi. This provided preliminary insights into its potential molecular mechanisms for treating PD, laying a foundation for the secondary development of other formulas.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231651","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":"Ginsenoside Rg2 Ameliorates Alzheimer's Disease by Alleviating Neuroinflammation in APP/PS1 Mice.","authors":"Dilida Yeerkenbieke, Yue Guan, Jing Cui, Qianqian Zhang, Gong Wang, Yifa Zhou, Zhiping Li, Chunyue Wang, Di Wang","doi":"10.2174/011570159X395496250911104139","DOIUrl":"https://doi.org/10.2174/011570159X395496250911104139","url":null,"abstract":"<p><strong>Introduction: </strong>Ginsenoside Rg2 (GRg2), a naturally occurring triterpenoid derived from ginseng rhizomes, exhibits neuroprotective properties. Neuroinflammation is recognized as one of the key pathogenic mechanisms underlying Alzheimer's disease (AD). This research aims to investigate the beneficial effects of GRg2 on AD and explore its potential mechanisms.</p><p><strong>Methods: </strong>In APP/PS1 mice, cognitive and behavioral assessments were first performed. Subsequently, brain tissue analyses were performed using immunohistochemical analysis and Western blot. A combined analysis of the gut microbiome and metabolomics was conducted to explore potential mechanisms. Finally, key findings were further validated through immunofluorescence and enzymelinked immunosorbent assay.</p><p><strong>Results: </strong>GRg2 enhanced learning, memory, and cognitive functions. And inhibits the deposition of β- amyloid and phosphorylated tau. GRg2 effectively inhibits the production of Bacteroides and Helicobacter. In addition, it reduced the levels of pyruvaldehyde and trimethylamine N-oxide, metabolites closely related to neuroinflammation. GRg2 effectively inhibited the activation of astrocytes and microglia in the brains of APP/PS1 mice, and also reduced the expression of neuroinflammatory mediators IL-6, IL-1β, and TNF-α.</p><p><strong>Discussions: </strong>The findings of this study substantiate the neuroprotective efficacy of GRg2, providing a novel therapeutic strategy and theoretical foundation for natural product-based interventions against AD.</p><p><strong>Conclusion: </strong>GRg2 improves cognitive function and mitigates AD pathology, which is at least partially attributed to its regulation of gut microbiota and metabolites, as well as its anti-neuroinflammatory effects.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198718","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":"Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.","authors":"Xingtong Shen, Hantao Chen, Jishan Zheng, Yunyan Ma, Zhengzhen Tang, Hongqin Sun, Qian Zhang, Jidong Zhang, Tao Song","doi":"10.2174/011570159X388747250830161230","DOIUrl":"https://doi.org/10.2174/011570159X388747250830161230","url":null,"abstract":"<p><p>Mitochondria play a critical role in immune cell differentiation, activation, and the regulation of innate immune responses. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a key mediator of cytosolic DNA sensing and contributes to a broad spectrum of pathological processes, including infectious diseases, sterile inflammation, cancer, and autoimmune disorders. STING is activated in response to cytosolic DNA during infection and can restrict translation in RNA virus-infected cells as part of the innate immune response. Studies have shown that mitochondrial dysfunction, particularly the release of mitochondrial DNA (mtDNA), can act as a potent trigger of cGAS-STING signaling, linking mitochondrial damage to immune activation. Additionally, this pathway intersects with autophagy, metabolic regulation, and cell death mechanisms. This comprehensive review summarizes current advances in understanding the cGAS-STING axis and mtDNA release in the context of mitochondrial dysfunction, with a focus on their roles in disease pathogenesis and potential as therapeutic targets. We highlight recent progress in the development of targeted interventions and emphasize the importance of elucidating the regulatory mechanisms underlying STING activation in various pathological conditions, including neuroinflammation, cancer, ischemia/reperfusion injury, and autoimmune diseases.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184955","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":"Neural Circuit Mechanisms of General Anaesthesia Induction: Current Advances and Future Directions.","authors":"Yanfang Yin, Yaxin Teng, Wenying Chi, Xinyuan Zhang, Haozhe Qiao, Xiaoyong Zhao, Meiyan Sun","doi":"10.2174/011570159X387168250912070856","DOIUrl":"https://doi.org/10.2174/011570159X387168250912070856","url":null,"abstract":"<p><p>General anaesthesia is traditionally divided into three distinct stages: induction, maintenance, and recovery. However, much of the existing literature has primarily focused on elucidating the mechanisms involved in the recovery phase, yielding several notable advancements. It is essential to recognize, however, that the induction and recovery phases represent two distinct processes. Studies in the induction phase have mainly centred on the impact of inhalational and intravenous anaesthetics on neural circuits, particularly those in the cortical and subcortical nuclei, as well as their specific effects on various neurotransmitters. Yet, the precise neural circuit mechanisms underlying anaesthetic induction still require further exploration. General anaesthetics influence neural circuitry by targeting neurons in particular nuclei, with their effects varying according to the distinct properties of individual anaesthetic agents. During the induction of anaesthesia, both the cortex and subcortical nuclei are significantly involved, with the inhibition of the subthalamic nucleus considered a core mechanism underlying this process. Notably, the periventricular thalamus, as part of the thalamus structure, holds particular importance in regulating the loss of consciousness. Additionally, the spinal cord and peripheral nervous system may play a potentially important role during the induction phase of general anaesthesia. Gaining a deeper understanding of the mechanisms underlying anaesthetic induction could reveal potential neuroanatomical targets that elucidate the alterations in consciousness during this phase of general anaesthesia. Such insights are invaluable in the quest for more effective, precise, and controllable anaesthetic practices, thereby enhancing the selection and combination of anaesthetic agents.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148094","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":"PGx-Based in silico Analyses Identifies the Interactive Role of Genes, Glucose Metabolism and Dopaminergic Dysfunctional Pathways with Chronic Cocaine use and Misuse.","authors":"Alireza Sharafshah, Panayotis K Thanos, Albert Pinhasov, Abdalla Bowirrat, Colin Hanna, Kai-Uwe Lewandrowski, Christopher Rowan, Igor Elman, Mark S Gold, Catherine A Dennen, Edward J Modestino, Rajendra D Badgaiyan, David Baron, Brian Fuehrlein, Ashim Gupta, Jean Lud Cadet, Aryeh R Pollack, Jag Khalsa, Milan Makale, Alexander Pl Lewandrowski, Kenneth Blum","doi":"10.2174/011570159X390146250831143523","DOIUrl":"https://doi.org/10.2174/011570159X390146250831143523","url":null,"abstract":"<p><strong>Introduction: </strong>Our team conducted a pharmacogenomics (PGx) analysis to evaluate the interactions between cocaine, glucose metabolism, and functional connectivity using in-depth silico PGx methods.</p><p><strong>Methods: </strong>Utilizing PharmGKB, we extracted PGx annotations related to cocaine, glucose, and dopamine (raw data). After filtering, we refined a list of 49 unrepeated, brain-expressed genes and examined their interactions in a protein-protein interaction (PPI) network through STRING-MODEL, identifying top candidate genes.</p><p><strong>Results: </strong>Targeting key protein-coding genes with the highest connectivity, we identified COMT, DRD2, and SLC6A3, along with their 17 connected genes. A deep dive into gene-miRNA interactions (GMIs) using NetworkAnalyst revealed that COMT, DRD2, and hsa-miR-16-5p have multiple interactions with OPRM1 and BDNF. Enrichment analysis via Enrichr confirmed that this refined set of 17 impacts dopamine function and are interactive with dopaminergic pathways. Notably, Substance Use disorders (SUD) were the most significant manifestation predicted for the interplays among these genes.</p><p><strong>Discussion: </strong>Reviewing all PGx annotations for the 17 genes, we found 4,665 PGx entries, among which 1,970 were significant, with a p-value above 0.045. These were ultimately filtered down to 32 potential PGx annotations excluded in association with \"Cocaine,\" \"Glucose or Diabetes,\" and \"Dopamine\". Accordingly, 12 Pharmacogenes represented 32 PGx-associated with Cocaine, Glucose, and Dopamine, including DRD2, COMT, OPRD1, OPRM1, SLC6A3, CHRNA5, CNR1, CYP2C19, DBH, GABRA2, NOS1AP, and SYT1.</p><p><strong>Conclusion: </strong>This in silico PGx analysis demonstrates strong, validated connections based on prior published data and robust computational predictions. Among the findings, the COMT gene was found to be the best-scoring gene here.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136630","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":"An Efficient Neuro-framework for Brain Tumor Classification Using a CNN-based Self-supervised Learning Approach with Genetic Optimizations.","authors":"Paripelli Ravali, Pundru Chandra Shaker Reddy, Pappula Praveen","doi":"10.2174/011570159X378103250806214613","DOIUrl":"https://doi.org/10.2174/011570159X378103250806214613","url":null,"abstract":"<p><strong>Introduction: </strong>Accurate and non-invasive grading of glioma brain tumors from MRI scans is challenging due to limited labeled data and the complexity of clinical evaluation. This study aims to develop a robust and efficient deep learning framework for improved glioma classification using MRI images.</p><p><strong>Methods: </strong>A multi-stage framework is proposed, starting with SimCLR-based self-supervised learning for representation learning without labels, followed by Deep Embedded Clustering to extract and group features effectively. EfficientNet-B7 is used for initial classification due to its parameter efficiency. A weighted ensemble of EfficientNet-B7, ResNet-50, and DenseNet-121 is employed for the final classification. Hyperparameters are fine-tuned using a Differential Evolution-optimized Genetic Algorithm to enhance accuracy and training efficiency.</p><p><strong>Results: </strong>EfficientNet-B7 achieved approximately 88-90% classification accuracy. The weighted ensemble improved this to approximately 93%. Genetic optimization further enhanced accuracy by 3-5% and reduced training time by 15%.</p><p><strong>Discussion: </strong>The framework overcomes data scarcity and limited feature extraction issues in traditional CNNs. The combination of self-supervised learning, clustering, ensemble modeling, and evolutionary optimization provides improved performance and robustness, though it requires significant computational resources and further clinical validation.</p><p><strong>Conclusion: </strong>The proposed framework offers an accurate and scalable solution for glioma classification from MRI images. It supports faster, more reliable clinical decision-making and holds promise for real-world diagnostic applications.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145112005","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":"Unraveling the Role of Perivascular Macrophages in Alzheimer's Disease: Insights from the Crosstalk between Immunometabolism and Ferroptosis.","authors":"Xiaolei Miao, Wei Yue, Jinxu Wang, Jiahui Chen, Lei Qiu, Halisa Paerhati, Qin Zhou, Pengyi Li, Anshi Wu, Minhao Zhang","doi":"10.2174/011570159X417328250908080404","DOIUrl":"https://doi.org/10.2174/011570159X417328250908080404","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Recent evidence increasingly supports a potential role of Perivascular Macrophages (PVMs), a unique subpopulation of brain immune cells, in the pathogenesis of Alzheimer's disease (AD). Strategically positioned at the brain-vasculature interface, PVMs sense the redox status, modulate immunity, and potentially influence ferroptosis-an iron-dependent form of regulated cell death increasingly implicated in AD. However, whether the involvement of PVMs in AD pathology specifically entails mechanisms related to the crosstalk between immunometabolism and ferroptosis, and the precise molecular pathways linking PVMs, immunometabolism, and ferroptosis to AD, remains unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We first obtained single-cell RNA sequencing data of PVMs from AD patients and control subjects via the GEO database, identified Differentially Expressed Genes (DEGs), and applied Mendelian Randomization (MR), with robustness validated via leave-one-out analysis to pinpoint key genes among the DEGs with causal relevance to AD. Next, we identified ferroptosis-related genes within these key genes and examined their associations with immune cell infiltration and immunometabolic signaling pathways, while also predicting their regulatory transcription factors to inform potential therapeutic strategies.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We identified 149 DEGs in PVMs between AD and control groups, which were primarily enriched in immune and metabolic pathways. MR analysis established eight genes (ACSL1, SPATA6, RAB31, NIBAN1, HDAC4, GRAMD1B, GCC2, and DENND3) as causally and negatively associated with AD risk (IVW analysis identified all P &lt; 0.05, with robustness confirmed by leave-one-out analysis), with ACSL1 being recognized as a known ferroptosis driver. Immune cell infiltration analysis revealed significant differences in monocyte and neutrophil proportions in AD, with DENND3 identified as the sole gene significantly correlated with monocyte abundance. The Key genes demonstrated distinct associations with immunometabolic pathways: GRAMD1B expression was positively associated with PI3K/AKT/mTOR signaling, whereas both NIBAN1 and SPATA6 showed enrichment in cells with high Notch signaling activity. ACSL1 exhibited robust associations with multiple pathways implicated in ferroptosis, including the IL-6/JAK/STAT3, interferon-γ, TGF-β, bile acid metabolism, and cholesterol homeostasis pathways, suggesting potential mechanisms that mediate the crosstalk between immunometabolism and ferroptosis. Transcription factor analysis highlighted shared regulation by CEBPD and the SP1/2/3/4 family, indicating convergent transcriptional control of these genes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This study identifies eight key genes in PVMs that may protect against AD through mechanisms involving the interplay between immunometabolism and ferroptosis. Our findings provide novel insights into the function of PVMs in AD pathophysiology and sugg","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145112019","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":"Myocardial Inflammation as Key Mediator of Heart-brain Interaction After Myocardial Ischemia/Infarction: Mechanistic Exploration of Post-Myocardial Infarction Cognitive Dysfunction.","authors":"Linhan Wang, Meng Mao, Hailong Bing, Wei Xu, Wangli Tian, Xuan Wang, Zhengyuan Xia, Qinjun Chu","doi":"10.2174/011570159X394212250825051955","DOIUrl":"https://doi.org/10.2174/011570159X394212250825051955","url":null,"abstract":"<p><p>Myocardial Infarction (MI) is a severe cardiovascular event, causing not only substantial damage to the heart but also potentially exerting a profound impact on brain function through a complex cardiac-brain interaction mechanism. The pathological process of MI encompasses myocardial cell necrosis, inflammatory cell infiltration, and the release of a substantial amount of inflammatory mediators. Through the bloodstream, these myocardial mediators may traverse the Blood-Brain Barrier (BBB), eliciting a neuroinflammatory response that can lead to cognitive dysfunction. This article proposes a critical research direction: investigating whether MI mediates the effects of myocardial- derived mediators on the permeability of the BBB, as well as the potential consequences of these mediators on cognitive functions. This review is aimed at triggering future research to elucidate the underlying mechanisms governing heart-brain interactions after MI in order to facilitate the development of more effective cognitive protection strategies for patients with MI.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079845","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":"Preface.","authors":"Ferdinando Nicoletti","doi":"10.2174/011570159X441819250909095415","DOIUrl":"https://doi.org/10.2174/011570159X441819250909095415","url":null,"abstract":"","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079798","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":"Advances in the Mechanism of ceRNA Regulation in Postoperative Cognitive Dysfunction.","authors":"Qiang Liu, Lin-Hui Ma, Chen-Rui Zhou, Tian-Qi Chen, Wei-Feng Wu, Hui-Hui Miao, Yu-Qing Wu, Cheng-Hua Zhou","doi":"10.2174/011570159X391415250707115740","DOIUrl":"https://doi.org/10.2174/011570159X391415250707115740","url":null,"abstract":"<p><p>Postoperative cognitive dysfunction (POCD) is a common central nervous system complication in elderly patients after surgery, characterized by cognitive changes, including impaired learning and memory, reduced attention, and mental disorders and personality changes in severe cases. Despite extensive research, effective targeted therapies remain elusive, underscoring the urgent need to elucidate their molecular mechanisms and identify novel therapeutic targets. Non-coding RNAs (ncRNAs), major transcription products of the human genome, are highly expressed in the central nervous system and play critical roles in regulating neuronal and synaptic complexity through interactions with other biomolecules. Notably, certain ncRNAs modulate gene expression networks by regulating miRNAs, a phenomenon known as the competing endogenous RNA (ceRNA) mechanism. In this review, we summarized and analyzed emerging evidence on ceRNA-mediated regulatory mechanisms in POCD pathogenesis, aiming to establish a foundation for future mechanistic exploration and therapeutic development.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063493","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}