Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-02-09DOI: 10.1016/j.brainresbull.2026.111772
Sujie Wang , Mengru Xu , Linze Qian , Lingyun Gao , Yu Sun
{"title":"Divergent effects of high-frequency rTMS on cognitive performance in sleep-deprived nurses: An EEG brain network study","authors":"Sujie Wang , Mengru Xu , Linze Qian , Lingyun Gao , Yu Sun","doi":"10.1016/j.brainresbull.2026.111772","DOIUrl":"10.1016/j.brainresbull.2026.111772","url":null,"abstract":"<div><h3>Background:</h3><div>Sleep deprivation (SD) is a common occupational hazard, particularly for shift workers like nurses, leading to significant impairments in cognitive functions such as sustained attention and working memory. High-frequency repetitive transcranial magnetic stimulation (rTMS) is a promising neuromodulation technique for cognitive enhancement, but its effects in sleep-deprived individuals and the underlying neural mechanisms remain poorly understood. This study aimed to investigate the efficacy of high-frequency rTMS over the left dorsolateral prefrontal cortex (DLPFC) in modulating sustained attention and working memory after a night shift and to explore the associated changes in brain network topology.</div></div><div><h3>Methods:</h3><div>In a within-subject design, 28 healthy female night-shift nurses participated in two experimental sessions after a night of work: one with real 5 Hz rTMS and one with sham rTMS applied to the left DLPFC. Following stimulation, participants performed a psychomotor vigilance task (PVT) and a 2-back task while their electroencephalography (EEG) data were recorded. Behavioral performance (reaction time and accuracy) and subjective fatigue were assessed. Graph theory analysis was applied to the EEG data to evaluate changes in functional brain network topology at both global and nodal levels.</div></div><div><h3>Results:</h3><div>Real rTMS significantly reduced subjective mental fatigue compared to sham stimulation. However, the behavioral effects were task-dependent. For the 2-back task, real rTMS led to a significant impairment in performance, characterized by slower reaction times and lower accuracy. For the PVT, there was a non-significant trend towards improved performance. These behavioral outcomes were mirrored by distinct patterns of network reorganization. During the PVT, real rTMS induced decreased functional segregation (lower clustering coefficient and local efficiency) in the alpha band. Conversely, during the 2-back task, it resulted in increased functional segregation and small-worldness in the theta band.</div></div><div><h3>Conclusion:</h3><div>High-frequency rTMS over the left DLPFC exerts differential, task-specific effects on cognitive function in a sleep-deprived state. The impairment in working memory, despite a network configuration theoretically supportive of local processing, likely results from an inverted-U effect, where the rTMS pushed an already strained and compensating brain system past its optimal level of cortical excitability. The findings highlight the critical role of both baseline brain state and specific cognitive demands in determining the outcomes of neuromodulation, providing crucial insights for the targeted application of rTMS to mitigate cognitive deficits from sleep deprivation.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111772"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146164100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-02-04DOI: 10.1016/j.brainresbull.2026.111766
Lin Xu , Ziyi Peng , Jie Lian , Xinxin Gong , Yongcong Shao , Mengfei Han , Fubin Jiao
{"title":"Stressed minds, altered strategies: Acute stress impairs proactive control in table tennis athletes","authors":"Lin Xu , Ziyi Peng , Jie Lian , Xinxin Gong , Yongcong Shao , Mengfei Han , Fubin Jiao","doi":"10.1016/j.brainresbull.2026.111766","DOIUrl":"10.1016/j.brainresbull.2026.111766","url":null,"abstract":"<div><h3>Background</h3><div>Intense stress greatly affects athletes’ mental state and performance, and cognitive control, which is vital for handling unexpected situations and maintaining peak performance. Although previous research has shown that acute stress can impact different aspects of cognitive control, the exact mechanisms and effects are still debated. This study aimed to investigate how acute stress impacts proactive and reactive control in table tennis players, providing new insights into the intricate role of stress in athletes’ cognitive control.</div></div><div><h3>Methods</h3><div>Acute stress was induced in 25 male table tennis athletes using the Maastricht Acute Stress Task (MAST). Behavioral and electroencephalogram (EEG) data were recorded before and after acute stress exposure. The EEG data included both resting-state and task-related recordings. Functional connectivity analysis was conducted on the resting-state EEG data. Event-related potential (ERP) analysis was conducted on the task-related EEG data recorded during the AX-Continuous Performance Task (AX-CPT).</div></div><div><h3>Results</h3><div>The behavioral results showed similar reaction times in table tennis athletes before and after acute stress, with AY trials showing significantly higher accuracy. The ERP results revealed a decrease in contingent negative variation (CNV) amplitude and increased N2 component but no significant difference was observed between the P3b and P3a components before and after acute stress. Functional connectivity analysis showed that acute stress activated the visual network and enhanced functional connectivity with multiple brain regions.</div></div><div><h3>Conclusion</h3><div>Acute stress induces large-scale activation of visual and salience networks while affecting the two modes of cognitive control, with reactive control predominating over proactive control. The weakening of proactive control by acute stress affected response preparation rather than pre-attention and stimuli processing, while the enhancement of reactive control resulted increased detection and monitoring of conflicting information. These findings shed light on how acute stress induces a neurocognitive shift in athletes, contributing to the advancement of the Dual Mechanisms of Cognitive Control (DMC) framework. This shift highlights the critical balance between proactive and reactive control under stress, offering valuable insights for developing interventions that optimize athletes’ performance under high-pressure conditions.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111766"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-01-31DOI: 10.1016/j.brainresbull.2026.111756
Xiaohu Xu , Jiaqi Hu , Yaxuan Wang , Yanyan Zhu , Yuwei Cao , Man Li , Ping Peng
{"title":"The central amygdala as a pathological hub: A multi-level review of pain–emotion comorbidity","authors":"Xiaohu Xu , Jiaqi Hu , Yaxuan Wang , Yanyan Zhu , Yuwei Cao , Man Li , Ping Peng","doi":"10.1016/j.brainresbull.2026.111756","DOIUrl":"10.1016/j.brainresbull.2026.111756","url":null,"abstract":"<div><div>Chronic pain frequently coexists with emotional disorders such as anxiety and depression, thereby imposing a considerable global burden. This review aims to establish the central amygdala (CeA) as the primary neural hub regulating pain-related comorbidities. Existing evidence demonstrates that the CeA shapes both the sensory-discriminative and emotional-motivational dimensions of pain by integrating ascending pain inputs and descending regulatory outputs. At the cellular level, functionally antagonistic GABAergic neuronal populations within the central lateral capsular division (CeLC) exhibit abnormal plasticity during chronic pain, which disrupts emotional homeostasis. Key molecular mechanisms within the CeA include neuropeptide signaling, regulation of ionotropic and metabotropic glutamate receptors, and opioid receptor dynamics, all of which often display lateralization and state dependence. Moreover, neuroimmune dysregulation within the CeA and epigenetic modifications contribute substantially to the persistence of pain–emotion comorbidities. By integrating evidence across neural circuits, cells, molecules, immune responses, and epigenetics, this multi-level review positions the CeA as a critical convergence point and promising therapeutic target for alleviating the intertwined suffering of chronic pain and emotional disorders.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111756"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146104049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-01-31DOI: 10.1016/j.brainresbull.2026.111758
Binfeng Tu , Yulong Ji , Zilong Tan , Shiqi Cheng , Yan Zhang
{"title":"Integrated transcriptomic analysis reveals mitochondrial dysregulation and macrophage heterogeneity associated with MTHFD2 in glioblastoma","authors":"Binfeng Tu , Yulong Ji , Zilong Tan , Shiqi Cheng , Yan Zhang","doi":"10.1016/j.brainresbull.2026.111758","DOIUrl":"10.1016/j.brainresbull.2026.111758","url":null,"abstract":"<div><h3>Background</h3><div>Glioblastoma (GBM) is an aggressive brain tumor with therapeutic resistance and poor prognosis. Mitochondrial dysfunction has emerged as a critical driver of tumor progression and immune modulation, yet mitochondrial gene alterations and their cellular specificity in GBM remain unclear.</div></div><div><h3>Methods</h3><div>Transcriptomic datasets (TCGA-GBM, GSE66354) were analyzed to identify differentially expressed mitochondria-associated genes using MitoCarta3.0. Prognostic mitochondrial DEGs (MitoDEGs) were determined by Cox regression, and a nomogram was constructed for survival prediction. Single-cell RNA sequencing was applied to explore mitochondrial gene expression in cellular populations, particularly macrophages. Functional enrichment and pseudotime analyses were conducted to define macrophage subpopulations, while in vitro assays validated the role of MTHFD2 in glioblastoma cell behavior, macrophage migration and the expression of IL-6 and CCL2.</div></div><div><h3>Results</h3><div>MTHFD2 was identified as a diagnosis mitochondrial hub gene strongly correlated with GBM diagnosis. Single-cell analysis revealed elevated mitochondrial activity and MTHFD2 expression in tumor-associated macrophages. A distinct MTHFD2-high macrophage subpopulation displayed immune-activated and metabolically reprogrammed pathways, representing a terminally differentiated state linked to tumor progression. Functional assays showed that silencing MTHFD2 suppressed glioblastoma cell proliferation, invasion, colony formation, and reduced macrophage migration and the expression of IL-6 and CCL2.</div></div><div><h3>Conclusion</h3><div>Mitochondrial dysfunction mediated by MTHFD2 in macrophages plays a key role in GBM progression and immune heterogeneity. MTHFD2 represents a potential diagnostic biomarker and therapeutic target for modulating GBM immune infiltration.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111758"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146104046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"HSP47 inhibitor Col003 inhibits glial scar formation and improves neurological function in ischemic stroke in rats","authors":"Kejian Zhou , Yuliang Xie , Xiaoyun Xie, Haoying Li, Tingting Liang, Jinpin Li, Jingli Liu","doi":"10.1016/j.brainresbull.2026.111745","DOIUrl":"10.1016/j.brainresbull.2026.111745","url":null,"abstract":"<div><h3>Background</h3><div>Glial scarring is a major obstacle for axonal regeneration and neural repair in the late stage of ischemic stroke. Reactive astrocytes are the main component of the glial scar. Heat shock protein 47 (HSP47) is significantly expressed in reactive astrocytes and remains present in the glial scar. However, the role of HSP47 in glial scar formation in ischemic stroke remains unclear.</div></div><div><h3>Methods</h3><div>HSP47 was identified in the peri-infarct region of rats at 1, 7, and 14 days post middle cerebral artery occlusion (MCAO). The rats received daily tail vein injections of the HSP47 inhibitor Col003 from days 1–14 following MCAO. Glial scar, brain atrophy volume, neurological score was detected after ischemia.</div></div><div><h3>Results</h3><div>HSP47 levels were increased in the peri-infarct area at 1, 7, and 14 days post-MCAO, as did those in astrocytes subjected to oxygen<img>glucose deprivation/reoxygenation (OGD/R). The HSP47 inhibitor Col003 enhanced neurological functional recovery and minimized glial scar formation. Col003 inhibited the proliferation and migration of OGD/R-induced astrocytes and reduced the expression of glial fibrillary acidic protein, neurocan, and phosphacan. RNA-seq analysis revealed that differentially expressed genes in the Col003 treatment group were enriched in the JAK2/STAT3 pathway, which is associated with astrogliosis and glial scar formation.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrated that Col003 inhibited JAK2/STAT3 phosphorylation in OGD/R-induced astrocytes. The HSP47 inhibitor Col003 might suppress astrocyte proliferation, migration, and glial scar formation through the JAK2/STAT3 pathway following ischemic stroke, which suggests a novel therapeutic strategy for the chronic phase of ischemic stroke.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111745"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146044021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-02-04DOI: 10.1016/j.brainresbull.2026.111765
Yue Yuan, Xun-Heng Wang
{"title":"The use of whole-brain network topology and weighted gene coexpression analysis to identify potential imaging and molecular markers for glioma grading","authors":"Yue Yuan, Xun-Heng Wang","doi":"10.1016/j.brainresbull.2026.111765","DOIUrl":"10.1016/j.brainresbull.2026.111765","url":null,"abstract":"<div><h3>Background</h3><div>Glioblastoma (GBM), which is characterized by high invasiveness and spatial heterogeneity, poses significant challenges in terms of prognosis and treatment. In this study, whole-brain network topology was combined with gene coexpression analysis to identify potential imaging and molecular markers for glioma grading, shifting the research focus from localized tumor lesions to the interaction mechanisms between the nervous system and gliomas.</div></div><div><h3>Methods</h3><div>In this study, data from open-access datasets, including glioma imaging data from the Brain Tumor Segmentation Challenge (BraTS’2019), data on glioma-related genes from BrainBase, and whole-brain transcriptomic data from the Allen Human Brain Atlas, were used. Wavelet-based features were extracted separately from T1- and T2-weighted magnetic resonance (MR) images and integrated to construct individualized structural brain networks with the aim of characterizing glioma heterogeneity. LASSO regression was applied to perform feature selection and extract the representative structural network metrics. We evaluated the effectiveness of the derived network features in glioma grading from this novel perspective via four classification models: support vector machine (SVM), random forest, logistic regression, and XGBoost. Furthermore, weighted gene coexpression network analysis (WGCNA) was employed to link disruptions in structural connectivity between high- and low-grade gliomas with the expression patterns of glioma-related genes, thereby identifying potential molecular markers associated with tumor progression.</div></div><div><h3>Results</h3><div>The results demonstrated that the whole-brain network-based grading approach achieved test-set AUC values above 0.85 across all four models, with the SVM and logistic regression models showing the best performance (AUC = 0.87). Additionally, the high invasiveness of high-grade gliomas may lead to the decoupling and reorganization of structural network modules. Protein kinase C beta (PRKCB) has been identified as a potential molecular biomarker associated with glioma grade.</div></div><div><h3>Conclusions</h3><div>Wavelet-based individualized brain structural networks have been proposed for glioma grading models, resulting in novel imaging and molecular markers for cancer neuroscience.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111765"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-02-04DOI: 10.1016/j.brainresbull.2026.111762
Lili Wang , Xinli Xiong , Baofeng Wang , Haiyu Li , Gang Li , Feifeng Liu
{"title":"Orexin dual receptor antagonist attenuates neurological deficits possibly via PI3K/Akt/mTOR pathway activation in sleep-deprived stroke rats","authors":"Lili Wang , Xinli Xiong , Baofeng Wang , Haiyu Li , Gang Li , Feifeng Liu","doi":"10.1016/j.brainresbull.2026.111762","DOIUrl":"10.1016/j.brainresbull.2026.111762","url":null,"abstract":"<div><h3>Background</h3><div>Post-stroke sleep disorders are frequent complications of ischemic stroke and contribute to poor neurological recovery. Dual orexin receptor antagonists (DORAs) promote sleep via mechanisms distinct from traditional hypnotics. This study investigated whether almorexant attenuates sleep deprivation (SD)-aggravated ischemic injury in rats and explored the its potential association with PI3K/Akt/mTOR signaling pathway.</div></div><div><h3>Methods</h3><div>Male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO), and were assigned to sham, MCAO, MCAO+SD, MCAO+SD+almorexant, or MCAO+SD+estazolam. Neurological function (Zea-Longa score, open-field test), infarct volume (TTC), histopathology (H&E), neuronal apoptosis (TUNEL), and PI3K/Akt/mTOR expression (Western blot, RT-qPCR) were assessed.</div></div><div><h3>Results</h3><div>SD exacerbated neurological deficits after MCAO, as reflected by higher Zea–Longa scores and impaired locomotor activity. Almorexant treatment was associated with improved behavioral performance and reduced histologic injury, neuronal apoptosis in sleep-deprived MCAO rats. At the molecular level, both almorexant and estazolam treatments were associated with upregulated PI3K, Akt, and mTOR expression at both protein and mRNA levels.</div></div><div><h3>Conclusion</h3><div>Almorexant was associated with attenuation of SD-exacerbated ischemic brain injury in rats, accompanied by alterations in PI3K/Akt/mTOR signaling, suggesting DORAs may have potential relevance for the management of post-stroke insomnia.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111762"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-02-04DOI: 10.1016/j.brainresbull.2026.111764
Xiaolin Sun , Yuan Chang , Xiaoyue Tan , Qing Zhang , Hao Sun , Shanzhen He , Fanghu Wang , Lijun Lu , Lei Jiang
{"title":"Deep learning-based one-stop 11C-CFT and 18F-FDG dual-tracer brain PET imaging protocol for Parkinson’s disease","authors":"Xiaolin Sun , Yuan Chang , Xiaoyue Tan , Qing Zhang , Hao Sun , Shanzhen He , Fanghu Wang , Lijun Lu , Lei Jiang","doi":"10.1016/j.brainresbull.2026.111764","DOIUrl":"10.1016/j.brainresbull.2026.111764","url":null,"abstract":"<div><div>This study explored using deep learning (DL) to separate short-interval staggered <sup>11</sup>C-CFT/<sup>18</sup>F-FDG brain PET images for Parkinson’s disease, aiming to reduce scan waiting time. A total of 67 patients performing <sup>11</sup>C-CFT and <sup>18</sup>F-FDG brain PET scans on separate days were retrospectively enrolled. A Swin UNETR model was trained to generate pseudo <sup>18</sup>F-FDG PET images from simulated dual-tracer sum images. The simulation assumed <sup>18</sup>F-FDG was administered at 80, 100, 120, or 200 min (∆t) after <sup>11</sup>C-CFT injection. Compared to actual <sup>18</sup>F-FDG images, the pseudo images showed high visual similarity across all ∆t intervals. Low average NMSE values (∼0.0004) and high average SSIM values (0.9991–0.9993) were consistently achieved across all Δt groups. Bland & Altman analysis of the whole brain region demonstrated low average SUVR bias across all Δt groups remained within ±0.001. Region-wise correlation analysis revealed strong correlations between actual and pseudo <sup>18</sup>F-FDG images across all Δt, with slopes ranging from 0.994 to 1.001, and all R<sup>2</sup>> 0.99. SUVmean, LBR and SNR values for pseudo <sup>18</sup>F-FDG images exhibited no statistically significant differences compared to actual <sup>18</sup>F-FDG images (<em>P</em> > 0.05). Dual-tracer PET images can be effectively separated using the DL model, yielding high-quality visual and semi-quantitative results when <sup>18</sup>F-FDG is injected immediately after the <sup>11</sup>C-CFT PET scan, thereby reducing patient wait time, improving patient comfort, and enhancing overall clinical efficiency.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111764"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brain Research BulletinPub Date : 2026-03-01Epub Date: 2026-02-08DOI: 10.1016/j.brainresbull.2026.111769
Daghan Piskin , Gjergji Cobani , Daniel Büchel , Tim Lehmann , Jochen Baumeister
{"title":"Brain complexity in motion: Multiscale entropy analysis on mobile EEG data to assess motor performance","authors":"Daghan Piskin , Gjergji Cobani , Daniel Büchel , Tim Lehmann , Jochen Baumeister","doi":"10.1016/j.brainresbull.2026.111769","DOIUrl":"10.1016/j.brainresbull.2026.111769","url":null,"abstract":"<div><div>Multiscale entropy (MSE) as a measure of brain complexity provides substantial insights into the adaptability of the brain. However, it is often applied to resting-state electroencephalography (EEG) or in static tasks. The current study assessed the reliability, validity and classification accuracy of MSE computed on mobile EEG data for linking brain complexity to motor performance within a kicking task. Eleven novice participants underwent repeated measurements to assess test-retest reliability, while the data from 15 novices and 15 football players were used to evaluate known-groups validity, convergent validity and classification accuracy. EEG data were recorded using 65 active electrodes and MSE estimates were computed for 64 time scales on preprocessed data. Results showed poor to excellent reliability for MSE estimates, exhibiting channel- and scale-specific variations, with reliability generally higher at fine-to-mid scales. Experts exhibited significantly lower entropy at coarse scales in left frontal and at fine scales in centroparietal regions compared to novices. Negative correlations were found between entropy estimates and kicking accuracy. Receiver operating characteristic curves of entropy estimates and their principal components demonstrated moderate to good classification accuracy between expertise levels. These findings suggest MSE as a promising metric for investigating brain complexity in movement contexts, revealing distinct patterns of complexity associated with motor performance. Future research across diverse tasks and populations is crucial to further elucidate this relationship and explore the applied potential of MSE.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111769"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Potential roles of metabolomic alterations in neuropathic pain: Evidence from In Vivo to clinical studies","authors":"Rattanaporn Khrueamun , Chanisa Thonusin , Nipon Chattipakorn , Siriporn Chattipakorn","doi":"10.1016/j.brainresbull.2026.111754","DOIUrl":"10.1016/j.brainresbull.2026.111754","url":null,"abstract":"<div><div>Neuropathic pain is a chronic condition often associated with damage to the somatosensory nervous system. The exact mechanistic understanding of neuropathic pain remains elusive. Metabolomics, an analytical approach used to assess metabolic alterations in various diseases, is a promising technique that can offer mechanistic insights into neuropathic pain. It may lead to the identification of novel therapeutic targets and biomarkers. Evidence from animal studies indicates that alterations in multiple metabolic pathways, including those involving amino acids, fatty acids, glycolysis intermediates, Krebs cycle metabolites, and eicosanoids, have been observed in models of neuropathic pain. Changes in several metabolites, including phosphatidylcholine, arachidonic acid derivatives, and amino acid levels, have also been found in models of neuropathic pain. These alterations have been associated with mitochondrial dysfunction, impaired maintenance of the myelin sheath, and increased pain signaling. In addition, clinical studies have demonstrated dysregulation of glutamate, choline, phospholipid, and glucose metabolism in patients with neuropathic pain. These metabolic disturbances contribute to neuronal hyperexcitability and persistent pain. Interestingly, modulation of specific metabolic pathways has been shown to alleviate neuropathic pain, as evidenced by both <em>in vivo</em> and clinical studies. Therefore, this comprehensive review aims to summarize and discuss the metabolomic alterations associated with neuropathic pain.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"236 ","pages":"Article 111754"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}