Brain Research Bulletin最新文献

{"title":"Enhancing brain plasticity: Functional near-infrared spectroscopy evidence for computerized working memory training in healthy adults","authors":"Yuntao Gao ,&nbsp;Peng Fang ,&nbsp;Wanying Xing ,&nbsp;Lingwei Zeng ,&nbsp;Hui Wang ,&nbsp;Xia Zhu ,&nbsp;Xiuchao Wang","doi":"10.1016/j.brainresbull.2025.111646","DOIUrl":"10.1016/j.brainresbull.2025.111646","url":null,"abstract":"<div><h3>Background</h3><div>Understanding the neural mechanisms underlying cognitive enhancement through training is a central goal in neuroscience. Although computerized working memory training (WMT) has shown promise, its effects on brain plasticity, particularly the interplay between intrinsic network organization and task-evoked activity, remain poorly characterized. This study aimed to investigate these effects using multimodal Functional near-infrared spectroscopy (fNIRS).</div></div><div><h3>Methods</h3><div>We employed a randomized controlled trial with a pre-post design to investigate the effects of an 8-week adaptive computerized WMT program in healthy young adults. fNIRS was used to assess both resting-state functional connectivity (RSFC) and prefrontal cortex activation during the n-back task. Behavioral outcomes were measured across near-transfer (updating, inhibition, switching) and far-transfer (visuospatial/phonological storage) domains.</div></div><div><h3>Results</h3><div>Behavioral results demonstrated that, compared with the control group, the WMT group exhibited significant improvements after training not only in near-transfer tasks (e.g., updating and shifting functions) but also in far-transfer tasks (e.g., visuospatial and phonological loop tasks). Neuroimaging findings revealed multifaceted functional remodeling. During the resting state, the WMT group showed a significant increase in functional connectivity between the premotor cortex and the bilateral dorsolateral prefrontal cortex (DLPFC), along with enhanced interhemispheric frontal connectivity. When performing the n-back task, the WMT group displayed a significant reduction in activation levels (measured by total hemoglobin, HBT) in the bilateral DLPFC after training, despite improved behavioral performance, reflecting higher \"neural efficiency\".</div></div><div><h3>Conclusions</h3><div>Collectively, these findings indicate that AWMT can not only effectively enhance cognitive abilities but also induce profound functional remodeling of the prefrontal network by strengthening resting-state network integration and optimizing task-state brain resource allocation. This study provides new evidence for understanding the neural mechanisms underlying cognitive training and highlights the utility of fNIRS as a powerful tool for tracking dynamic changes in brain plasticity.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111646"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562792","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":"Progranulin deficiency exacerbates postoperative cognitive dysfunction via RhoA-mediated axodendritic impairment in aged mice","authors":"Yini Lu ,&nbsp;Xinyu Tian ,&nbsp;Chun Yang ,&nbsp;Dan Wang ,&nbsp;Ya Yan ,&nbsp;Gang Wang ,&nbsp;Xiaofeng Lei","doi":"10.1016/j.brainresbull.2025.111649","DOIUrl":"10.1016/j.brainresbull.2025.111649","url":null,"abstract":"<div><h3>Background</h3><div>Postoperative cognitive dysfunction (POCD) is a debilitating complication in surgical patients, especially the elderly. yet its molecular mechanisms remain inadequately understood. This study investigates the effects of progranulin (PGRN) on hippocampal neuronal damage and cognitive impairment induced by surgical trauma.</div></div><div><h3>Methods</h3><div>Aged mice underwent laparotomy to model POCD, and cognitive function was assessed using the Morris Water Maze and Novel Object Recognition tests. Molecular changes were identified through RNA sequencing. Hippocampal neuronal integrity was evaluated with immunofluorescence, Golgi staining, and transmission electron microscopy. In vitro, HT22 neurons exposed to lipopolysaccharide (LPS) were treated with recombinant PGRN or RhoA-overexpressing lentivirus to investigate mechanistic pathways.</div></div><div><h3>Results</h3><div>Surgery significantly decreased PGRN expression in hippocampal neurons, which was associated with axonal and dendritic damage, cytoskeletal disorganization, and cognitive decline. In LPS-treated HT22 cells, loss of PGRN impaired neurite outgrowth, while exogenous PGRN restored neurite extension by inhibiting RhoA activation. Overexpression of RhoA reversed PGRN’s neuroprotective effects. In vivo, intrahippocampal PGRN administration reduced neuroinflammation, improved axodendritic function, and enhanced cognitive performance in POCD mice.</div></div><div><h3>Conclusion</h3><div>PGRN deficiency drives POCD pathogenesis via RhoA-mediated cytoskeletal dysfunction. Therapeutic targeting of the PGRN-RhoA axis presents a novel strategy to preserve neuronal connectivity and mitigate postoperative cognitive decline in aging populations.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111649"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585622","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":"Presynaptic BDNF-TrkB signaling contributes to mechanical allodynia in a mouse model of chronic neuropathic pain","authors":"Ting Ding ,&nbsp;Lanying Zhang ,&nbsp;Jingqing Xu ,&nbsp;Maomao Liu ,&nbsp;Yao Ou-Yang ,&nbsp;Sheng Liu","doi":"10.1016/j.brainresbull.2025.111625","DOIUrl":"10.1016/j.brainresbull.2025.111625","url":null,"abstract":"<div><div>In the spinal cord, brain-derived neurotrophic factor (BDNF) exerts its regulatory role on neuropathic pain through its receptor TrkB. This study constructed a conditional TrkB gene knockout mouse model, targeting all nociceptive neurons (SNS^Cre;TrkB^fl/fl) or all sensory neurons (Advillin^Cre;TrkB^fl/fl) in the dorsal root ganglia (DRG), to investigate the function of presynaptic BDNF-TrkB signaling in the dorsal horn and its impact on specific sensory modalities. In situ hybridization (ISH) was used to detect TrkB expression in nociceptive SNS^tdTomato neurons, revealing that TrkB is expressed in both sensory neurons and nociceptors in the DRG. Triple immunofluorescence techniques were employed to detect the co-expression of neuron-specific markers NF200, CGRP, and IB4 with TrkB mRNA, and the co-expression ratios were analyzed. To assess motor function and aversive behavior, CatWalk (CW), home cage (HC), and wheel rotation (W<em>R</em>) tests were conducted; basic pain and touch sensitivity were evaluated using von Frey, cotton swabs, brush, pinprick, acetone, cold plate, Hargreaves, and hot plate tests, as well as tapping and hair clamp tests, with no effects observed on neurodevelopment, motor function, or aversive behavior. In addition, this study used the CCI model to conduct behavioral tests related to nerve injury in SNS^Cre;TrkB^fl/fl and Advillin^Cre;TrkB^fl/fl mice. After CCI surgery, both mouse strains exhibited severe dynamic and punctate mechanical allodynia deficits, while thermal and cold allodynia developed normally. Ultimately, by administering exogenous BDNF via intrathecal (IT) injection, mechanical allodynia deficits were observed in Advillin^Cre;TrkB^fl/fl and SNS^Cre;TrkB^fl/fl mice. The results confirmed that TrkB is expressed presynaptically and plays a role in the development of dynamic and punctate mechanical allodynia during BDNF-induced spinal plasticity responses, but has no effect on thermal or cold allodynia. In conjunction with previous studies, these findings suggest that BDNF may partially regulate presynaptic inhibition following nerve injury through TrkB.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111625"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145480671","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":"Machine learning and deep learning in clinical practice: Advancing neurodegenerative disease diagnosis with multimodal markers","authors":"Omid Zarei ,&nbsp;Maryam Talebi moghaddam ,&nbsp;Sadegh Moradi Vastegani","doi":"10.1016/j.brainresbull.2025.111667","DOIUrl":"10.1016/j.brainresbull.2025.111667","url":null,"abstract":"<div><div>Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, present major global health challenges due to their progressive and incurable nature. Early and accurate diagnosis is critical to slow disease progression and optimize therapeutic interventions, yet conventional diagnostic approaches, such as neuroimaging, cerebrospinal fluid biomarker analysis, and clinical evaluation are often inadequate at the prodromal stage. Recent advances in artificial intelligence, particularly machine learning (ML), have provided new opportunities for precision diagnosis and treatment in neurology, using large data and multimodal biomarkers. Applications of ML to data from neuroimaging, electrophysiology, behavioral functions, speech and handwriting analysis, and molecular biomarkers have shown promising improvements in diagnostic accuracy, patient classification, and therapeutic recommendations. However, significant challenges remain, including data heterogeneity, model interpretability, population diversity, and ethical concerns surrounding patients’ privacy. The purpose of this review is to examine current applications of ML in the diagnosis and management of neurodegenerative diseases through various data, highlight its strengths and limitations, and discuss future directions for using these approaches in clinical practice. We also outline emerging directions, including multimodal fusion with longitudinal data, federated and privacy-preserving learning, and the potential of explainable AI (XAI) and large language models (LLMs) in clinical decision support.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111667"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145667113","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":"Salvianolic acid A prevented neuroinflammation and apoptosis caused by acute ischemic stroke through inhibiting the HMGB1/NF-κB signaling pathway","authors":"Chengdi Liu ,&nbsp;Sen Zhang ,&nbsp;Aiping Wen ,&nbsp;Linglei Kong ,&nbsp;Guanhua Du","doi":"10.1016/j.brainresbull.2025.111657","DOIUrl":"10.1016/j.brainresbull.2025.111657","url":null,"abstract":"<div><div>Neuroinflammation plays a role in the overall pathophysiological process of stroke. Developing preventive stroke drugs that target neuroinflammation may be a promising strategy. The aim of our study was to investigate the effect of salvianolic acid A (SAA) administered preventively on the regulation of neuroinflammation and apoptosis and to evaluate its underlying mechanisms during stroke. An autologous thrombus stroke model was established in SD rats using electrocoagulation, and an oxygen-glucose deprivation (OGD) injury model was created in human brain microvascular endothelial cells (HBMECs). SAA (10 mg/kg) was administered orally twice a day for 5 days prior to the operation. The supernatant of lipopolysaccharide (LPS) -treated BV2 cells was used as conditioned medium (CM). HBMECs were co-cultured with CM for 6 h. Our results showed that pretreatment with SAA alleviated cerebral infarction, decreased the levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α), inhibited the polarization of M1 microglia, promoted the polarization of M2 microglia, inhibited apoptosis, and balanced the expression of Bax and Bcl-2 proteins both in vivo and in vitro. Furthermore, we found that SAA inhibited the activation of the HMGB1/NF-κB signaling pathway. In conclusion, our results indicate that SAA prevents neuroinflammation and apoptosis caused by acute ischemic stroke through the inhibition of the HMGB1/NF-κB signaling pathway. Pretreatment with SAA is a potential strategy for the prevention of ischemic stroke.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111657"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145630184","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":"Task-specific effects of sleep deprivation on cognitive function and EEG brain network in night-shift nurses","authors":"Jingjia Yuan ,&nbsp;Mengru Xu ,&nbsp;Linze Qian ,&nbsp;Lingyun Gao ,&nbsp;Yu Sun","doi":"10.1016/j.brainresbull.2025.111661","DOIUrl":"10.1016/j.brainresbull.2025.111661","url":null,"abstract":"<div><h3>Background:</h3><div>Night-shift nurses experience chronic sleep deprivation, which impairs cognitive functions crucial for patient safety. However, the underlying reorganization of brain functional networks remains poorly understood. This study aimed to investigate the task-specific effects of sleep deprivation on brain network topology during sustained attention and working memory in night-shift female nurses.</div></div><div><h3>Methods:</h3><div>In a within-subjects design, electroencephalography (EEG) data from 28 female nurses were recorded during a rested session (R-Session) and a sleep-deprived session (SD-Session) immediately following a night shift. Participants performed the psychomotor vigilance test (PVT) and 2-back tasks. Functional connectivity was estimated using the weighted phase lag index (wPLI), and brain network properties were quantified using graph theoretical analysis at both global and nodal levels.</div></div><div><h3>Results:</h3><div>Our findings revealed a clear behavioral dissociation: sleep deprivation significantly impaired PVT performance but had no effect on 2-back task performance. This dissociation was mirrored by distinct patterns of neural reorganization. During the PVT, the brain network exhibited a compensatory enhancement of global topology, characterized by a significant increase in clustering coefficient, global efficiency, local efficiency, and small-worldness, alongside a decrease in characteristic path length, particularly in the theta and beta bands. In contrast, the 2-back task showed only a localized increase in the theta-band clustering coefficient. Nodal analysis further revealed a critical topographical distinction: PVT-related efficiency changes were strongly right-lateralized, whereas 2-back changes were bilaterally distributed.</div></div><div><h3>Conclusion:</h3><div>In conclusion, these results demonstrate that sleep deprivation elicits task-specific neurocognitive adaptations. Sustained attention appears highly vulnerable, prompting a broad compensatory reorganization of the right-hemispheric attention network. Conversely, working memory function remains behaviorally stable, underpinned by a more specific network reorganization, primarily involving increased local connectivity. This study deepens our understanding of the neural mechanisms underlying cognitive vulnerability and resilience in nurses group.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111661"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660245","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":"Structural and functional abnormalities of thalamic subregions in minimal hepatic encephalopathy","authors":"Li-Min Cai ,&nbsp;Shao-Peng Zhuang ,&nbsp;Zi-Wei Cai ,&nbsp;Ying Tang ,&nbsp;Si-Yuan Fang ,&nbsp;Dan Li ,&nbsp;Jian-Qi Li ,&nbsp;Hua-Jun Chen","doi":"10.1016/j.brainresbull.2025.111654","DOIUrl":"10.1016/j.brainresbull.2025.111654","url":null,"abstract":"<div><h3>Purpose</h3><div>The thalamus, which consists of multiple subregions, has been of particular interest in the study of minimal hepatic encephalopathy (MHE). This study aimed to identify abnormalities of the thalamic subregions in patients with MHE and their associations with cognitive performance.</div></div><div><h3>Methods</h3><div>Two groups of patients—30 patients with cirrhosis with MHE (the MHE group) and 48 patients with cirrhosis without MHE (the NHE group)—and 42 healthy controls (the HC group) underwent resting-state functional and structural magnetic resonance imaging. A histologically based atlas was used to segment the thalamus into 25 nuclei and subsequently group the thalamus into 6 subregions. Volume and mean regional homogeneity (mReHo, metrics reflecting local brain activity) were assessed in six thalamic subregions per hemisphere and the entire thalamus, and group differences were analyzed. Correlation analyses were conducted to explore associations between neuroimaging changes and clinical performance.</div></div><div><h3>Results</h3><div>The MHE group showed increased volume in the bilateral posterior thalamic subregions (false-discovery rate [FDR]-corrected <em>P</em> &lt; 0.05). Functionally, the MHE group showed increased mReHo values in the bilateral posterior, bilateral intralaminar, and left ventral thalamic subregions (FDR-corrected <em>P</em> &lt; 0.05). Notably, both significant structural and functional alterations showed a progressive increase from NHE group to MHE group. These alterations in the thalamic subregions of patients with cirrhosis were significantly correlated with performance on neurocognitive tests (FDR-corrected <em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Our findings support the role of thalamic subregional alterations in the pathophysiology of MHE and highlight their potential as neuroimaging markers for early detection of MHE-related cognitive decline.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111654"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145596176","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":"Decoding sepsis-associated encephalopathy: From blood–brain barrier injury to mechanism-based subphenotypes","authors":"Qin Song,&nbsp;Bo Song","doi":"10.1016/j.brainresbull.2025.111660","DOIUrl":"10.1016/j.brainresbull.2025.111660","url":null,"abstract":"<div><div>Sepsis-associated encephalopathy (SAE) is a frequent but underrecognized complication of systemic infection, characterized by acute brain dysfunction and long-term cognitive impairment in the absence of direct central nervous system infection. Despite its high morbidity and mortality, the mechanistic basis of SAE remains poorly defined, limiting early diagnosis and targeted intervention. This review synthesizes recent advances in the molecular and cellular pathophysiology of SAE, with emphasis on blood–brain barrier (BBB) disruption, neuroinflammation, glial cell activation, mitochondrial dysfunction, and neurotransmitter imbalance. We highlight the central role of BBB breakdown in facilitating peripheral-to-central immune signaling, which triggers a cascade of neuroinflammatory and metabolic events that collectively disrupt synaptic homeostasis and neuronal integrity. Emerging evidence also supports the existence of biologically distinct SAE subphenotypes, such as ischemic-hypoxic, inflammatory-dominant, and metabolic-degenerative types—each associated with specific molecular features and clinical outcomes. These insights underscore the need for biomarker-driven patient stratification and mechanism-targeted therapeutic strategies. Future research should prioritize the development of integrated diagnostic platforms, molecular phenotyping tools, and neuroprotective therapies that address the heterogeneous nature of SAE. A refined understanding of its pathogenesis holds promise for transforming the clinical management of SAE and improving long-term neurological recovery in sepsis survivors.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111660"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615518","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":"Radiomics of the midbrain on TCCD for identifying Parkinson’s disease in substantia nigra hyperechogenicity-negative individuals","authors":"Zhirong Xu ,&nbsp;Jiayi Ye ,&nbsp;Xiaoqian Zhang ,&nbsp;Jiemin Chen ,&nbsp;Han Wang ,&nbsp;Qichen Su ,&nbsp;Yanru Li","doi":"10.1016/j.brainresbull.2025.111651","DOIUrl":"10.1016/j.brainresbull.2025.111651","url":null,"abstract":"<div><div>This study evaluated the diagnostic utility of midbrain radiomic features from transcranial color Doppler (TCCD) imaging for identifying Parkinson’s disease (PD) in individuals without substantia nigra hyperechogenicity (SN−). A total of 61 SN− PD patients and 61 age- and sex-matched SN− healthy controls were retrospectively enrolled after excluding subjects with visible hyperechogenicity or poor image quality. Midbrain regions of interest were manually segmented, and 464 radiomic features were extracted. Feature selection was performed using the Mann–Whitney U test with FDR correction and LASSO regression, followed by training of four machine learning models with five-fold cross-validation and independent testing. SHAP analysis was applied for model interpretation. All models performed well in the training set (e.g., XGBoost AUC = 0.96, SVM AUC = 0.91), but only the support vector machine (SVM) maintained stable performance on the test set, achieving an AUC of 0.79, accuracy of 0.74, and F1-score of 0.75. In contrast, XGBoost and random forest showed reduced performance, suggesting overfitting. Based on its consistent and balanced results, SVM was selected as the optimal classifier. SHAP analysis identified DependenceVariance, HighGrayLevelZoneEmphasis, ZoneVariance, and GrayLevelNonUniformity as the most influential features, reflecting heterogeneity, gray-level variability, and high-intensity zone prominence in the SN− PD group. These findings demonstrate that radiomics applied to midbrain TCCD images can identify PD in the absence of conventional ultrasound markers, providing an interpretable, noninvasive approach that may complement current diagnostic strategies.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111651"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585687","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":"Effect of estrogens on sex-specific influence in sleep deprivation in mice","authors":"Qi Deng ,&nbsp;Yuhong Li ,&nbsp;Zuoli Sun ,&nbsp;Xue Fenqin ,&nbsp;Xiang Gao ,&nbsp;Rena Li","doi":"10.1016/j.brainresbull.2025.111663","DOIUrl":"10.1016/j.brainresbull.2025.111663","url":null,"abstract":"<div><div>Men and women generally exhibit different sleep patterns and structures. These differences also extend to how each sex responds to sleep deprivation, a condition linked to various health issues. Although estradiol is known to influence sleep patterns, its sex-specific effects on sleep characteristics and the responses to sleep deprivation are not well understood. In our study, we used a genetic estrogen deficiency mouse model with aromatase deficiency (Ar^+/-) to explore estrogens’ sex-specific role in reactions to acute sleep deprivation (SD). Initially, we identified a sex difference in SD-induced sleep-wake proportions and sleep patterns in wild type (WT) mice. Then, we found that estrogens deficiency caused alterations of normal sleep pattern in females, characterized by less wakefulness and more NREM time, but not in males at baseline compared to WT mice. While SD led to significant alterations in circadian rhythm, sleep patterns, and sleep rebound in both male and female Ar^+/- mice, sex differences were evident in specific responses to SD. Female Ar^+/- mice exhibited a quicker and longer-lasting post-SD sleep rebound, with reduced wake time, increased sleep time, and less fragmented sleep, whereas male Ar^+/- mice showed a delayed sleep rebound except for REM sleep time and REM sleep spectral alterations compared to WT mice. Our findings underscore the crucial role of endogenous estrogens in sleep regulation and its sex-specific response to sleep deprivation, which could be significant for precision sleep medicine.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"233 ","pages":"Article 111663"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145630020","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}