Journal of integrative neuroscience最新文献

{"title":"Remote Ischemic Conditioning Attenuates Apoptosis, the Inflammatory Response, and Reperfusion Injury in Ischemic-Stroke Model Rats via the ELA-Apelin-APJ System.","authors":"Feng Zhou, Yangyang Wu, Xuan Chen, Zhuoli Pan, Xiaolong Wang, Shengwei Gao, Chenle Shi, Jie Ren, Jing Shi","doi":"10.31083/JIN39897","DOIUrl":"https://doi.org/10.31083/JIN39897","url":null,"abstract":"<p><strong>Background: </strong>Remote ischemic conditioning (RIC), a novel neuroprotective therapy, has broad potential for reducing the occurrence and recurrence of cerebrovascular events, yet its mechanisms are not incompletely understood. The aim of this study is to investigate whether RIC alleviates apoptosis, inflammation, and reperfusion injury in rat models of ischemic stroke by regulating the Elabela (ELA)-apelin-Apelin receptor (APJ) system.</p><p><strong>Methods: </strong>We established a rat model of middle cerebral artery occlusion (MCAO) with ischemia-reperfusion injury, and RIC was administered twice daily for 3 days post-MCAO. Cerebral infarct volume was measured and neuronal damage was assessed. Apoptosis-related caspase-3 expression was detected by Terminal deoxynucleotidyl Utransferase nick-End Labeling (TUNEL) and Western blotting (WB). WB was also used to measure apelin, signal transducer and activator of transcription 3 (STAT3), and p-STAT3 protein levels in infarcted brain tissue. ELA miRNA expression was evaluated. Immunofluorescence was used to detect hypoxia-inducible factor 1α (HIF-1α) and activating transcription factor 4 (ATF4) expression. Serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured using enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>RIC reduced the cerebral infarct volume and neuronal damage in MCAO rats. Compared with the MCAO group, the RIC-treated group (MCAO+RIC) presented significantly lower caspase-3, TNF-α, IL-1β, p-STAT3, HIF-1α, and ATF4 expression (<i>p</i> < 0.05), whereas STAT3 and ELA miRNA expression and apelin protein levels were increased (<i>p</i> < 0.05). While positively correlated with STAT3 expression, Elabela and apelin levels exhibited a negative correlation with caspase-3 (<i>p</i> < 0.05).</p><p><strong>Conclusions: </strong>RIC mitigates MCAO-induced neuronal apoptosis, inflammation, and reperfusion injury by modulating the ELA-apelin-APJ system, highlighting its therapeutic potential for ischemic stroke.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"39897"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction to the Physiology, Anatomy, and Biochemistry of Autonomic Medicine.","authors":"Forrest Sturgill, Kamal Shouman, Paola Sandroni","doi":"10.31083/JIN31369","DOIUrl":"10.31083/JIN31369","url":null,"abstract":"<p><p>Autonomic medicine is a rapidly evolving field focused on understanding diseases and processes that affect the autonomic nervous system (ANS). The ANS regulates essential involuntary physiologic processes such as heart rate, blood pressure, and digestion. This review introduces the key anatomical structures, physiological mechanisms, and biochemical processes underlying autonomic function. The anatomy section focuses on the peripheral components of the ANS, including the sympathetic and parasympathetic divisions. The physiological section explores the process of homeostasis and the intricate feedback systems that maintain this balance within the body. Finally, the biochemistry of autonomic signaling, focusing on the neurotransmitters acetylcholine, norepinephrine, and epinephrine, and their receptors, is reviewed. Pertinent clinical points are highlighted throughout, emphasizing the importance of the basic science to the clinical world. This review aims to provide a comprehensive basic science foundation for clinicians and researchers exploring the field of autonomic medicine.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"31369"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of the DPP4 Inhibitor Sitagliptin on Ferroptosis in Epilepsy.","authors":"Baohua Hou, Lin Li, Fei Wang, Jincheng Guo","doi":"10.31083/JIN39469","DOIUrl":"https://doi.org/10.31083/JIN39469","url":null,"abstract":"<p><strong>Background: </strong>Epilepsy, a significant neurological condition marked by the occurrence of repeated seizures, continues to pose a substantial health challenge. Previous studies have indicated that Dipeptidyl Peptidase-4 (DPP4) inhibitors may possess antiepileptic properties. Ferroptosis, a newly discovered type of programmed cell death, has recently surfaced as a promising therapeutic target in the management of epilepsy. Nevertheless, the exact mechanisms responsible for the effects of DPP4 inhibitors have not yet been fully elucidated.</p><p><strong>Methods: </strong>The anti-epileptic effect was evaluated through electroencephalogram (EEG) recordings, behavioral assessments, and immunohistochemical analysis in a mouse model of epilepsy induced by LiCl/Pilocarpine. Public RNA-sequencing data was used to search the key targets of epilepsy. Neuronal ferroptosis was assessed through western blotting and immunofluorescence in an epilepsy rat model and a glutamate-induced neuronal cell model.</p><p><strong>Results: </strong>Administration of the DPP4 inhibitor sitagliptin was observed to markedly reduce seizure severity in an animal model of epilepsy. Furthermore, sitagliptin effectively diminished epileptiform activity, as assessed by EEG. Additionally, pretreatment with sitagliptin led to a notable decrease in the expression of heme oxygenase-1 (HO-1), reactive oxygen species (ROS) production, and mitochondrial damage, while increasing glutathione peroxidase 4 (GPX4) expression in the epilepsy rat model. Similar effects were observed in cell-based experiments, where sitagliptin pretreatment enhanced GPX4 expression in glutamate-induced neuronal models.</p><p><strong>Conclusions: </strong>The DPP4 inhibitor sitagliptin mitigates ferroptosis in epilepsy models. These findings highlight new potential targets and treatment modalities for epilepsy.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"39469"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic Insights and Translational Therapeutics of Neurovascular Unit Dysregulation in Vascular Cognitive Impairment.","authors":"Li-Shan Lin, Yu-Qi Huang, Jia-Yi Xu, Jun-Ming Han, Sheng Wu, Yin-Zhi Jin, Chao Han, Wei-Kang Hu, Zi-Xuan Xu, Takuya Sasaki, Chu Tong, Ying-Mei Lu","doi":"10.31083/JIN40091","DOIUrl":"https://doi.org/10.31083/JIN40091","url":null,"abstract":"<p><p>Cognitive impairment represents a progressive neurodegenerative condition with severity ranging from mild cognitive impairment (MCI) to dementia and exerts significant burdens on both individuals and healthcare systems. Vascular cognitive impairment (VCI) represents a heterogeneous clinical continuum, spanning a spectrum from subcortical ischemic VCI (featuring small vessel disease, white matter lesions, and lacunar infarcts) to mixed dementia, where vascular and Alzheimer's-type pathologies coexist. While traditionally linked to macro- and microvascular dysfunction, the mechanisms underlying VCI remain complex. However, contemporary research has gone beyond structural vascular damage, highlighting the neurovascular unit (NVU) as a critical mediator. Emerging evidence demonstrates that cerebral endothelial cells within the NVU not only regulate oxygen and nutrient transport but also orchestrate neuroinflammatory signaling and neurovascular coupling (NVC). Crucially, endothelial dysfunction initiates a self-perpetuating cycle of NVU dysregulation characterized by: (1) NVC impairment through diminished nitric oxide bioavailability and calcium signaling defects, (2) blood-brain barrier (BBB) breakdown via tight-junction protein degradation and pericyte detachment, and (3) neuroinflammation driven by endothelial-derived cytokine release and leukocyte infiltration. By integrating recent advances in NVU biology, we have established a framework to inform clinical strategies for early diagnosis and targeted therapies, which we outline in this review. Moreover, proactive management of vascular risk factors (e.g., hypertension, diabetes) in presymptomatic stages may mitigate the progression from vascular injury to irreversible dementia, underscoring its preventive potential. These insights reinforce the idea that preserving NVU integrity represents a pivotal approach to mitigating the global dementia burden.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"40091"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EEG-ERnet: Emotion Recognition based on Rhythmic EEG Convolutional Neural Network Model.","authors":"Shuang Zhang, Chen Ling, Jingru Wu, Jiawen Li, Jiujiang Wang, Yuanyu Yu, Xin Liu, Jujian Lv, Mang I Vai, Rongjun Chen","doi":"10.31083/JIN41547","DOIUrl":"10.31083/JIN41547","url":null,"abstract":"<p><strong>Background: </strong>Emotion recognition from electroencephalography (EEG) can play a pivotal role in the advancement of brain-computer interfaces (BCIs). Recent developments in deep learning, particularly convolutional neural networks (CNNs) and hybrid models, have significantly enhanced interest in this field. However, standard convolutional layers often conflate characteristics across various brain rhythms, complicating the identification of distinctive features vital for emotion recognition. Furthermore, emotions are inherently dynamic, and neglecting their temporal variability can lead to redundant or noisy data, thus reducing recognition performance. Complicating matters further, individuals may exhibit varied emotional responses to identical stimuli due to differences in experience, culture, and background, emphasizing the necessity for subject-independent classification models.</p><p><strong>Methods: </strong>To address these challenges, we propose a novel network model based on depthwise parallel CNNs. Power spectral densities (PSDs) from various rhythms are extracted and projected as 2D images to comprehensively encode channel, rhythm, and temporal properties. These rhythmic image representations are then processed by a newly designed network, EEG-ERnet (Emotion Recognition Network), developed to process the rhythmic images for emotion recognition.</p><p><strong>Results: </strong>Experiments conducted on the dataset for emotion analysis using physiological signals (DEAP) using 10-fold cross-validation demonstrate that emotion-specific rhythms within 5-second time intervals can effectively support emotion classification. The model achieves average classification accuracies of 93.27 ± 3.05%, 92.16 ± 2.73%, 90.56 ± 4.44%, and 86.68 ± 5.66% for valence, arousal, dominance, and liking, respectively.</p><p><strong>Conclusions: </strong>These findings provide valuable insights into the rhythmic characteristics of emotional EEG signals. Furthermore, the EEG-ERnet model offers a promising pathway for the development of efficient, subject-independent, and portable emotion-aware systems for real-world applications.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"41547"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperphosphorylated Tau Induces Cortical Hypoexcitability in Transgenic Mouse Models: A Meta-Analysis.","authors":"Carlos A García-Carlos, Gustavo Basurto-Islas, George Perry, Cesar Campos-Ramírez, Siddhartha Mondragón-Rodríguez","doi":"10.31083/JIN39192","DOIUrl":"10.31083/JIN39192","url":null,"abstract":"<p><strong>Background: </strong>Neurofibrillary tangles, composed of hyperphosphorylated tau, have been implicated in the cognitive impairments observed in Alzheimer's disease. While the precise mechanism remains elusive, cognitive deficits in Alzheimer's disease have been associated with disrupted brain network activity. To investigate this mechanism, researchers have developed several tau transgenic models. However, the extent of variability in cortical network alterations across different genetic backgrounds and ages is still not clearly defined.</p><p><strong>Objective: </strong>To evaluate the oscillatory alterations in relation to animal developmental age and hyperphosphorylated tau protein accumulation, we reviewed and analyzed the published data on peak power and quantification of theta-gamma cross-frequency coupling (modulation index values).</p><p><strong>Methods: </strong>A systematic review was conducted to locate and extract all studies published from January, 2002 to March, 2024 involving <i>in vivo</i> cortical local field potential recording in tau transgenic mouse models, ensuring the most current search results. Our meta-analysis was conducted following the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines.</p><p><strong>Results: </strong>The presence of hyperphosphorylated tau was associated with oscillatory alterations primarily reflected in power decreases, while modulation index values did not exhibit significant alterations.</p><p><strong>Conclusions: </strong>In this analysis, we uncovered that neuronal oscillations in cortical networks are altered from the prodromal to late stages of pathology. Additionally, we found that hyperphosphorylated tau accumulation is strongly associated with cortical network hypoexcitability in tau transgenic models.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"39192"},"PeriodicalIF":2.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Low Sodium Diet Activates HSD2 Neurons in the Nucleus Tractus Solitarii to Promote Sodium Appetite Via the cAMP/MAPK Signaling Pathway.","authors":"Xue Zhao, Yongqiang Chen, Ke Zhao, Yanxuan Wei, Yongan Zhang, Kun Liu, Luo Shi","doi":"10.31083/JIN42286","DOIUrl":"https://doi.org/10.31083/JIN42286","url":null,"abstract":"<p><strong>Background: </strong>Sodium homeostasis is crucial for physiological balance, yet the neurobiological mechanisms underlying sodium appetite remain incompletely understood. The nucleus tractus solitarii (NTS) integrates visceral signals to regulate feeding behaviors, including sodium intake. This study investigated the role of 11β-hydroxysteroid dehydrogenase type 2 (HSD2)-expressing neurons in the NTS in mediating sodium appetite under low-sodium diet (LSD) conditions and elucidated the molecular pathways involved, particularly the cyclic adenosine monophosphate (cAMP)/mitogen-activated protein kinase (MAPK) signaling cascade.</p><p><strong>Methods: </strong>Using a murine model, sodium preference was assessed via a two-bottle choice test following LSD exposure. Previously published single-cell RNA sequencing data were re-analyzed to profile the transcriptional changes in HSD2 neurons. Pharmacological interventions employed MAPK inhibitor U0126 and cAMP inhibitor KH7 to dissect signaling contributions. Anterograde tracing and immunohistochemistry techniques were used to verify the efferent projections of HSD2 neurons. Autonomic function was evaluated by measuring blood pressure (BP), heart rate (HR), and phrenic nerve discharge (PND) parameters in anesthetized mice during HSD2 neuron activation.</p><p><strong>Results: </strong>LSD significantly activated HSD2 neurons and increased sodium intake. scRNA-seq analysis revealed upregulation of genes in the cAMP/MAPK pathways under LSD conditions. Pharmacological blockade of these pathways abolished LSD-induced sodium appetite. Anterograde tracing confirmed three primary downstream targets: the pre-locus coeruleus (pre-LC), lateral parabrachial nucleus (PBcL), and ventral lateral bed nucleus of the stria terminalis (vlBNST). Notably, HSD2 neuron activation did not alter BP, HR, or PND parameters, indicating no direct role in autonomic regulation.</p><p><strong>Conclusions: </strong>LSD induces the activation of HSD2 neurons, which in turn causes sodium intake, a phenomenon that is eliminated by blocking the cAMP/MAPK signaling pathway. These neurons project to key forebrain and brainstem regions implicated in motivational behavior but do not directly modulate cardiovascular/respiratory functions. By replicating and extending prior research, this study supports and expands the present understanding of this field.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"42286"},"PeriodicalIF":2.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ciprofol Regulates the Activity of Mitochondrial Respiratory Chain Complex I During Cerebral Ischemia-Reperfusion by Targeting Flavin Mononucleotide: A Metabolomic Study.","authors":"Jixin Chen, Guoyou Chen, Yueheng Wu, Shuai Liu, Yifan Ma, Maonan Liu, Wei Yu","doi":"10.31083/JIN40079","DOIUrl":"https://doi.org/10.31083/JIN40079","url":null,"abstract":"<p><strong>Background and purpose: </strong>Ciprofol, a novel intravenous anesthetic, has been shown to exert protective effects against ischemic stroke, a leading cause of death and disability; however, its molecular mechanisms remain unclear. This study aimed to explore the molecular mechanisms underlying the neuroprotective effects of ciprofol using metabolomics.</p><p><strong>Methods: </strong>This study used a middle cerebral artery occlusion (MCAO) rat model to simulate cerebral ischemia-reperfusion injury (CIRI). The rats were divided into ciprofol, MCAO, and sham groups. Histological and neurobehavioral testing methods were used to investigate the therapeutic effects of ciprofol in rats. Ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry was used to screen for differential metabolites and related metabolic pathways in the serum and brain of the three groups. Spectrophotometry was used to detect <i>in vitro</i> mitochondrial respiratory chain complex I (MRCC-I) activity.</p><p><strong>Results: </strong>Neurological behavioral scores and cerebral infarct volumes of rats in the ciprofol group were significantly lower than those of rats in the MCAO group. Metabolomic analysis revealed 19 differential metabolites in serum samples and 31 differential metabolites in brain samples, including flavin mononucleotide (FMN). These metabolites were mainly enriched in the tricarboxylic acid cycle, respiratory electron transport chain, and amino acid and lipid metabolism. <i>In vitro</i> experiments demonstrated that ciprofol promoted the activity of MRCC-I during CIRI by increasing FMN levels.</p><p><strong>Conclusion: </strong>The mechanisms of action of ciprofol during treatment of cerebral ischemia involve the tricarboxylic acid cycle, respiratory electron transport chain, and amino acid and lipid metabolism and may directly affect MRCC-I activity by regulating FMN.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"40079"},"PeriodicalIF":2.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Brain-Gut-Microbiome Axis Across the Life Continuum and the Role of Microbes in Maintaining the Balance of Health.","authors":"Tyler Halverson, Kannayiram Alagiakrishnan","doi":"10.31083/JIN36616","DOIUrl":"https://doi.org/10.31083/JIN36616","url":null,"abstract":"<p><p>There is a growing body of evidence that the interaction between various microbial organisms and the human host can affect various physical and even mental health conditions. Bidirectional communication occurs between the brain and the gut microbiome, referred to as the brain-gut-microbiome axis. During aging, changes occur to the gut microbiome due to various events and factors such as the mode of delivery at birth, exposure to medications (e.g., antibiotics), environmental exposures, diet, and host genetics. Connections to the brain-gut-microbiome axis through different systems also change during aging, leading to the development of chronic diseases. Disruption of the gut microbiome, known as dysbiosis, can lead to a reduction in beneficial bacteria and a corresponding increase in more harmful or even pathogenic bacteria. This imbalance may predispose or contribute to the development of various health conditions and illnesses. Targeted treatment of the gut microbiome and the brain-gut-microbiome axis may assist in the overall management of these various ailments. The purpose of this review is to describe the changes that occur in the gut microbiome throughout life, and to highlight the risk factors for microbial dysbiosis. We discuss the different health conditions experienced at various stages of life, and how dysbiosis may contribute to the clinical presentation of these diseases. Modulation of the gut microbiome and the brain-gut-microbiome axis may therefore be beneficial in the management of various ailments. This review also explores how various therapeutics may be used to target the gut microbiome. Gut biotics and microbial metabolites such as short chain fatty acids may serve as additional forms of treatment. Overall, the targeting of gut health may be an important strategy in the treatment of different medical conditions, with nutritional modulation of the brain-gut-microbiome axis also representing a novel strategy.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"36616"},"PeriodicalIF":2.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the Influence of Emotion and Fatigue on Cognitive Function During Simulated Flight Based on ERP Technology.","authors":"Ruikai Zhao, Pengyan Zhou, Jinhan Liu, Yixuan Guan, Jiacheng Qian, Jiayi Bao","doi":"10.31083/JIN38435","DOIUrl":"10.31083/JIN38435","url":null,"abstract":"<p><strong>Background: </strong>Pilots often experience mental fatigue during task performance, accompanied by fluctuations in positive (e.g., joy) and negative (e.g., tension) emotions. Both mental fatigue and emotional changes significantly contribute to aviation accidents, yet few studies have considered their interplay. This study had three primary objectives. First, it examined the changes in positive and negative emotions following mental fatigue. Second, it investigated how these emotions influence the recovery from fatigue. Finally, it developed a comprehensive evaluation model integrating mental fatigue and emotional states.</p><p><strong>Methods: </strong>Two task sets were created using the visual search paradigm, incorporating simulated flight tasks with positive and negative emotional stimuli. Data were collected from 30 participants using electroencephalogram (EEG), eye-tracking, electrocardiogram (ECG), and behavioral performance metrics.</p><p><strong>Results: </strong>Participants showed mental fatigue after the simulated flight task, with reduced arousal for both positive and negative emotions; positive images had stronger effects. ERP showed decreased N1, P3, and LPP amplitudes. A Support Vector Machine (SVM) classifier achieved over 93% accuracy for fatigue but about 70% for emotion recognition.</p><p><strong>Conclusions: </strong>The task effectively induced fatigue and indicated that positive stimuli may aid recovery. Multimodal features support accurate fatigue detection, though emotion classification needs improvement Clinical Trial Registration: No: ChiCTR2500104961. https://www.chictr.org.cn/showproj.html?proj=267844.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"38435"},"PeriodicalIF":2.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}