Jun-ying Li, Jun Li, Zhong-jiao Lu, Wen Zhou, Yan-hui Li, Yong-jiang Luo, Xue-min Zhong, Jian Wang, Jing Gou, Lan-ying He
Background and purpose:
Intravenous thrombolysis (IVT) and endovascular thrombectomy (EVT) are primary treatments for acute ischemic stroke (AIS), but their efficacy is limited. This study aims to evaluate the short-term predictive value of the neutrophil-to-lymphocyte ratio (NLR) in AIS patients undergoing reperfusion therapies.
Method
AIS patients who underwent IVT and/or EVT at Chengdu Second People's Hospital were continuously enrolled from January 2020 to September 2024. NLR was calculated from blood samples taken before treatment. Primary outcomes were functional status at discharge (assessed using the modified Rankin Scale [mRS]), while secondary outcomes included in-hospital mortality and any intracranial hemorrhage (ICH). Statistical analyses included logistic regression and receiver operating characteristic (ROC) curve analysis.
Results
Among 817 patients, 327 (40.0%) exhibited poor functional outcomes at discharge. NLR positively correlated with the National Institutes of Health Stroke Scale score (ρ = 0.298, p < 0.001). Univariate analysis showed a significant association between NLR and poor functional outcomes at discharge, higher in-hospital mortality, and increased ICH incidence. After adjusting for confounders, NLR remained an independent predictor of functional outcomes (odds ratio 1.092; 95% confidence interval [CI] 1.006–1.185; p = 0.036). ROC analysis showed that NLR could predict functional outcomes with a cutoff value of 3.66 and an area under the curve of 0.679 (95% CI 0.641–0.717, p < 0.001).
Conclusions
NLR is an independent predictor of short-term functional outcomes and complications in AIS patients receiving reperfusion therapies, serving as a valuable tool for early prognosis and clinical decision-making.
背景与目的：静脉溶栓（IVT）和血管内取栓（EVT）是急性缺血性脑卒中（AIS）的主要治疗方法，但其疗效有限。本研究旨在评估中性粒细胞与淋巴细胞比值（NLR）在AIS患者再灌注治疗中的短期预测价值。方法：自2020年1月至2024年9月，连续招募成都市第二人民医院行静脉内腔和/或EVT的AIS患者。NLR根据治疗前采集的血液样本计算。主要结局是出院时的功能状态（使用改进的Rankin量表[mRS]评估），而次要结局包括住院死亡率和颅内出血（ICH）。统计分析包括logistic回归和受试者工作特征（ROC）曲线分析。结果：在817例患者中，327例（40.0%）在出院时表现为功能不良。NLR与美国国立卫生研究院卒中量表评分呈正相关（ρ = 0.298, p < 0.001）。单因素分析显示NLR与出院时不良功能结局、较高住院死亡率和脑出血发生率增加之间存在显著关联。在调整混杂因素后，NLR仍然是功能结局的独立预测因子（优势比1.092；95%可信区间[CI] 1.006-1.185; p = 0.036）。ROC分析显示NLR可以预测功能结局，截断值为3.66，曲线下面积为0.679 （95% CI 0.641-0.717, p < 0.001）。结论：NLR是AIS患者接受再灌注治疗的短期功能结局和并发症的独立预测指标，是早期预后和临床决策的重要工具。
{"title":"Neutrophil-to-Lymphocyte Ratio as an Independent Predictor of Adverse Short-Term Functional Outcomes After Reperfusion Therapy in Acute Ischemic Stroke","authors":"Jun-ying Li, Jun Li, Zhong-jiao Lu, Wen Zhou, Yan-hui Li, Yong-jiang Luo, Xue-min Zhong, Jian Wang, Jing Gou, Lan-ying He","doi":"10.1002/brb3.71122","DOIUrl":"10.1002/brb3.71122","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and purpose:</h3>\u0000 \u0000 <p>Intravenous thrombolysis (IVT) and endovascular thrombectomy (EVT) are primary treatments for acute ischemic stroke (AIS), but their efficacy is limited. This study aims to evaluate the short-term predictive value of the neutrophil-to-lymphocyte ratio (NLR) in AIS patients undergoing reperfusion therapies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>AIS patients who underwent IVT and/or EVT at Chengdu Second People's Hospital were continuously enrolled from January 2020 to September 2024. NLR was calculated from blood samples taken before treatment. Primary outcomes were functional status at discharge (assessed using the modified Rankin Scale [mRS]), while secondary outcomes included in-hospital mortality and any intracranial hemorrhage (ICH). Statistical analyses included logistic regression and receiver operating characteristic (ROC) curve analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 817 patients, 327 (40.0%) exhibited poor functional outcomes at discharge. NLR positively correlated with the National Institutes of Health Stroke Scale score (<i>ρ</i> = 0.298, <i>p</i> < 0.001). Univariate analysis showed a significant association between NLR and poor functional outcomes at discharge, higher in-hospital mortality, and increased ICH incidence. After adjusting for confounders, NLR remained an independent predictor of functional outcomes (odds ratio 1.092; 95% confidence interval [CI] 1.006–1.185; <i>p</i> = 0.036). ROC analysis showed that NLR could predict functional outcomes with a cutoff value of 3.66 and an area under the curve of 0.679 (95% CI 0.641–0.717, <i>p</i> < 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>NLR is an independent predictor of short-term functional outcomes and complications in AIS patients receiving reperfusion therapies, serving as a valuable tool for early prognosis and clinical decision-making.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71122","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
André Felipe dos Santos, Gabriel Chaves de Melo, Gabriela Castellano, Arturo Forner-Cordero
Background
Coincidence anticipation timing (CAT) tasks require individuals to synchronize their movement with an external moving stimulus. Electroencephalography (EEG), due to its high temporal resolution, offers a valuable tool for investigating the neural processes underlying temporal anticipation in these tasks.
Objectives
This scoping review aims to map the existing literature on EEG monitoring of temporal anticipation during CAT tasks, identify methodological patterns, evaluate the consistency of reported EEG markers, and highlight potential gaps.
Eligibility criteria
Studies were included if they examined EEG activity related to anticipatory processes during CAT tasks in human participants.
Sources of evidence
Studies were obtained from PubMed, Web of Science, and Scopus. A systematic search was conducted in May 2024 and updated in October 2025.
Charting methods
Data were charted across studies, focusing on participant characteristics, protocols, EEG methodologies, and reported outcomes.
Results
Eleven studies met our criterion. Substantial methodological variability was identified in participant setup, task design, EEG acquisition, and data analysis strategies. Although some EEG markers have been recurrently explored, no neural features were consistently assessed across all studies, limiting the identification of robust markers of temporal anticipation. Reporting gaps were observed regarding participant characteristics, anticipation type, and error metrics.
Conclusions
The field remains exploratory, with considerable heterogeneity across studies. To support more reliable comparisons and advance progress, this review proposes practical methodological recommendations focused on standardizing CAT task design and EEG procedures. These guidelines aim to enhance research quality and contribute to a more cohesive understanding of the neural correlates of temporal anticipation.
背景：巧合预期时间（CAT）任务要求个体与外部运动刺激同步运动。脑电图（EEG）由于其高时间分辨率，为研究这些任务中潜在的时间预期的神经过程提供了有价值的工具。目的：本综述旨在对CAT任务中时间预期的脑电图监测的现有文献进行梳理，确定方法模式，评估已报道的脑电图标记物的一致性，并突出潜在的差距。入选标准：如果研究对象在CAT任务中检测了与预期过程相关的脑电图活动，则纳入研究。证据来源：研究来自PubMed、Web of Science和Scopus。2024年5月进行了系统搜索，并于2025年10月更新。制图方法：将各研究的数据绘制成图表，重点关注参与者特征、方案、脑电图方法和报告结果。结果：11项研究符合我们的标准。在参与者设置、任务设计、脑电图采集和数据分析策略方面发现了大量的方法差异。尽管一些脑电图标记物已经被反复探索，但所有研究都没有一致地评估神经特征，这限制了对时间预期的稳健标记物的识别。在参与者特征、预期类型和错误度量方面观察到报告差距。结论：该领域仍处于探索性阶段，研究之间存在相当大的异质性。为了支持更可靠的比较和推进进展，本综述提出了实用的方法建议，重点是标准化CAT任务设计和EEG程序。这些指导方针旨在提高研究质量，并有助于对时间预期的神经相关性有更有凝聚力的理解。
{"title":"EEG Monitoring of Temporal Anticipation in Coincidence Anticipation Timing Tasks: A Scoping Review With Recommendations","authors":"André Felipe dos Santos, Gabriel Chaves de Melo, Gabriela Castellano, Arturo Forner-Cordero","doi":"10.1002/brb3.71123","DOIUrl":"10.1002/brb3.71123","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Coincidence anticipation timing (CAT) tasks require individuals to synchronize their movement with an external moving stimulus. Electroencephalography (EEG), due to its high temporal resolution, offers a valuable tool for investigating the neural processes underlying temporal anticipation in these tasks.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This scoping review aims to map the existing literature on EEG monitoring of temporal anticipation during CAT tasks, identify methodological patterns, evaluate the consistency of reported EEG markers, and highlight potential gaps.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Eligibility criteria</h3>\u0000 \u0000 <p>Studies were included if they examined EEG activity related to anticipatory processes during CAT tasks in human participants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Sources of evidence</h3>\u0000 \u0000 <p>Studies were obtained from PubMed, Web of Science, and Scopus. A systematic search was conducted in May 2024 and updated in October 2025.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Charting methods</h3>\u0000 \u0000 <p>Data were charted across studies, focusing on participant characteristics, protocols, EEG methodologies, and reported outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Eleven studies met our criterion. Substantial methodological variability was identified in participant setup, task design, EEG acquisition, and data analysis strategies. Although some EEG markers have been recurrently explored, no neural features were consistently assessed across all studies, limiting the identification of robust markers of temporal anticipation. Reporting gaps were observed regarding participant characteristics, anticipation type, and error metrics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The field remains exploratory, with considerable heterogeneity across studies. To support more reliable comparisons and advance progress, this review proposes practical methodological recommendations focused on standardizing CAT task design and EEG procedures. These guidelines aim to enhance research quality and contribute to a more cohesive understanding of the neural correlates of temporal anticipation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71123","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The main objective of this study is to non-invasively investigate the relationship between metacognitive beliefs and cortisol, the primary stress output of the hypothalamic-pituitary-adrenal (HPA) axis, as well as neurotrophic factors associated with neuroplasticity brain-derived neurotrophic factor and neuron-derived neurotrophic factor (BDNF and NDNF). Within this framework, the hypotheses that negative metacognitions would be associated with increased cortisol and decreased BDNF levels, and that cortisol might play a mediating role in this relationship, were tested.
Method
The study was designed in a cross-sectional model with 60 university students. Participants' metacognitive beliefs were measured using the Metacognitions Questionnaire-30 (MCQ-30). Salivary cortisol, BDNF, and NDNF levels were analyzed using the ELISA method. Pearson correlation and hierarchical multiple regression analyses were used for data analysis.
Finding
The results showed a significant positive relationship between the total metacognition score and cortisol (r = 0.589, p < 0.01) and a strong negative relationship between cortisol and BDNF (r = −0.662, p < 0.01). Hierarchical regression analysis supported a partial mediation model, indicating that dysfunctional metacognitive beliefs have both a significant direct negative association with BDNF and an indirect association mediated by cortisol. In the final model, both metacognition (β = –0.298, p < 0.05) and cortisol (β = –0.281, p < 0.05) were significant factors associated with lower BDNF levels. NDNF showed a positive relationship with BDNF (r = 0.571) but not with other variables.
Conclusion
These findings point to a psychobiological model where dysfunctional metacognitive beliefs are linked to suppressed neuroprotective mechanisms like BDNF, both directly and indirectly through HPA axis activation. The results shed light on the potential neurobiological mechanisms underlying the effectiveness of metacognitive therapies.
目的：本研究的主要目的是无创研究元认知信念与皮质醇、下丘脑-垂体-肾上腺（HPA）轴的初级应激输出以及与神经可塑性脑源性神经营养因子和神经元源性神经营养因子（BDNF和NDNF）相关的神经营养因子之间的关系。在这个框架内，消极元认知与皮质醇增加和BDNF水平下降有关的假设得到了检验，皮质醇可能在这种关系中起中介作用。方法：采用横断面模型对60名大学生进行研究。使用元认知问卷-30 （MCQ-30）测量参与者的元认知信念。采用ELISA法分析各组唾液皮质醇、BDNF、NDNF水平。数据分析采用Pearson相关分析和分层多元回归分析。结果发现：元认知总分与皮质醇呈显著正相关（r = 0.589, p < 0.01），皮质醇与BDNF呈显著负相关（r = -0.662, p < 0.01）。层次回归分析支持部分中介模型，表明功能失调的元认知信念与BDNF有显著的直接负相关，也有皮质醇介导的间接关联。在最终模型中，元认知（β = -0.298, p < 0.05）和皮质醇（β = -0.281, p < 0.05）是与BDNF水平降低相关的显著因素。NDNF与BDNF呈正相关（r = 0.571），与其他变量无关。结论：这些发现指向了一个心理生物学模型，其中功能失调的元认知信念与抑制的神经保护机制（如BDNF）直接或间接地通过HPA轴激活联系在一起。这些结果揭示了元认知疗法有效性的潜在神经生物学机制。
{"title":"The Relationship Between Metacognitive Beliefs and Salivary Cortisol, BDNF, and NDNF Levels: A Cross-Sectional Study","authors":"Süheyb Okur, Bülent Bayraktar, Fatma Tosun Köse","doi":"10.1002/brb3.71063","DOIUrl":"10.1002/brb3.71063","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>The main objective of this study is to non-invasively investigate the relationship between metacognitive beliefs and cortisol, the primary stress output of the hypothalamic-pituitary-adrenal (HPA) axis, as well as neurotrophic factors associated with neuroplasticity brain-derived neurotrophic factor and neuron-derived neurotrophic factor (BDNF and NDNF). Within this framework, the hypotheses that negative metacognitions would be associated with increased cortisol and decreased BDNF levels, and that cortisol might play a mediating role in this relationship, were tested.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>The study was designed in a cross-sectional model with 60 university students. Participants' metacognitive beliefs were measured using the Metacognitions Questionnaire-30 (MCQ-30). Salivary cortisol, BDNF, and NDNF levels were analyzed using the ELISA method. Pearson correlation and hierarchical multiple regression analyses were used for data analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Finding</h3>\u0000 \u0000 <p>The results showed a significant positive relationship between the total metacognition score and cortisol (<i>r</i> = 0.589, <i>p</i> < 0.01) and a strong negative relationship between cortisol and BDNF (<i>r</i> = −0.662, <i>p</i> < 0.01). Hierarchical regression analysis supported a partial mediation model, indicating that dysfunctional metacognitive beliefs have both a significant direct negative association with BDNF and an indirect association mediated by cortisol. In the final model, both metacognition (<i>β</i> = –0.298, <i>p</i> < 0.05) and cortisol (<i>β</i> = –0.281, <i>p</i> < 0.05) were significant factors associated with lower BDNF levels. NDNF showed a positive relationship with BDNF (<i>r</i> = 0.571) but not with other variables.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings point to a psychobiological model where dysfunctional metacognitive beliefs are linked to suppressed neuroprotective mechanisms like BDNF, both directly and indirectly through HPA axis activation. The results shed light on the potential neurobiological mechanisms underlying the effectiveness of metacognitive therapies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71063","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, posing a significant challenge to global public health. As a core signaling pathway in the mammalian innate immune system, the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a pivotal role in maintaining intracellular homeostasis. This review aims to systematically elucidate the role and therapeutic potential of the cGAS-STING signaling pathway in AD, focusing on its involvement in key pathological processes and its relevance to AD risk factors.
Method
Through literature search, we summarized the molecular mechanisms of the cGAS-STING pathway and its dysregulation in AD, emphasizing the integrated evidence linking cGAS-STING to neuroinflammation, autophagy impairment, and neuronal death, as well as its interactions with aging, obesity, cardiovascular disease, and diabetes.
Findings
The cGAS-STING pathway is critically involved in AD pathogenesis, contributing to neuroinflammation, defective autophagy, and neuronal loss. Its activation is associated with multiple AD risk factors, suggesting a broad influence on disease progression. Pharmacological inhibition of cGAS-STING shows promise in attenuating these pathological features in preclinical models.
Conclusion
The cGAS-STING signaling pathway plays a central regulatory role in the central nervous system, and its dysregulation promotes neuroinflammation and is closely associated with AD. This pathway forms a vicious cycle by integrating multiple pathological signals, including mitochondrial dysfunction and endoplasmic reticulum stress. Small-molecule inhibitors and natural products targeting this pathway have demonstrated significant efficacy in preclinical studies, providing a basis for developing disease-modifying therapies for AD. Future efforts should focus on multi-target combination strategies (e.g., STING inhibitors co-administered with Aβ/tau drugs) and dynamically deciphering pathway alterations across AD stages to advance personalized treatment approaches.
{"title":"The Role and Therapeutic Potential of the cGAS-STING Signaling Pathway in Alzheimer's Disease","authors":"Xue Li, Wei Gao, Qiuyan Ye, Honglin Li","doi":"10.1002/brb3.71130","DOIUrl":"10.1002/brb3.71130","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, posing a significant challenge to global public health. As a core signaling pathway in the mammalian innate immune system, the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a pivotal role in maintaining intracellular homeostasis. This review aims to systematically elucidate the role and therapeutic potential of the cGAS-STING signaling pathway in AD, focusing on its involvement in key pathological processes and its relevance to AD risk factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>Through literature search, we summarized the molecular mechanisms of the cGAS-STING pathway and its dysregulation in AD, emphasizing the integrated evidence linking cGAS-STING to neuroinflammation, autophagy impairment, and neuronal death, as well as its interactions with aging, obesity, cardiovascular disease, and diabetes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Findings</h3>\u0000 \u0000 <p>The cGAS-STING pathway is critically involved in AD pathogenesis, contributing to neuroinflammation, defective autophagy, and neuronal loss. Its activation is associated with multiple AD risk factors, suggesting a broad influence on disease progression. Pharmacological inhibition of cGAS-STING shows promise in attenuating these pathological features in preclinical models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The cGAS-STING signaling pathway plays a central regulatory role in the central nervous system, and its dysregulation promotes neuroinflammation and is closely associated with AD. This pathway forms a vicious cycle by integrating multiple pathological signals, including mitochondrial dysfunction and endoplasmic reticulum stress. Small-molecule inhibitors and natural products targeting this pathway have demonstrated significant efficacy in preclinical studies, providing a basis for developing disease-modifying therapies for AD. Future efforts should focus on multi-target combination strategies (e.g., STING inhibitors co-administered with Aβ/tau drugs) and dynamically deciphering pathway alterations across AD stages to advance personalized treatment approaches.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andreata, V. G., R. P. D. Freitas, J. da S. Nascimento, et al. 2025. “Genetic Basis of the Negative Response to the Use of Triptans for the Treatment of Migraine—A Systematic Review and Meta-Analysis.” Brain and Behavior 15, no. 10: e70967. https://doi.org/10.1002/brb3.70967
In the published version, the following funding information was missing:
Funding: The authors were partially supported by the Coordenação de Aperfeiçoamento de PessoaI de Nível Superior (CAPES), Finance Code 88881.015383/2024-01, under Process number 1466/2025.
We apologize for this error.
安德雷塔，V. G.， R. P. D. Freitas， J. da . S. Nascimento等。2025。使用曲坦类药物治疗偏头痛负面反应的遗传基础——系统回顾和荟萃分析。大脑与行为，第15卷，不。10: e70967。在已发布的版本https://doi.org/10.1002/brb3.70967In中，缺少以下资金信息：资金：作者部分由Nível高级（CAPES）协调机构（CAPES）资助，财务代码88881.015383/2024-01，流程号1466/2025。我们为这个错误道歉。
{"title":"Correction to “Genetic Basis of the Negative Response to the Use of Triptans for the Treatment of Migraine—A Systematic Review and Meta-Analysis”","authors":"","doi":"10.1002/brb3.71067","DOIUrl":"10.1002/brb3.71067","url":null,"abstract":"<p>Andreata, V. G., R. P. D. Freitas, J. da S. Nascimento, et al. 2025. “Genetic Basis of the Negative Response to the Use of Triptans for the Treatment of Migraine—A Systematic Review and Meta-Analysis.” <i>Brain and Behavior</i> 15, no. 10: e70967. https://doi.org/10.1002/brb3.70967</p><p>In the published version, the following funding information was missing:</p><p>Funding: The authors were partially supported by the Coordenação de Aperfeiçoamento de PessoaI de Nível Superior (CAPES), Finance Code 88881.015383/2024-01, under Process number 1466/2025.</p><p>We apologize for this error.</p>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The COVID-19 pandemic has coincided with marked increases in anxiety and depressive disorders. Beyond infection risks, socioeconomic stressors such as rising unemployment and stringent government responses may have contributed substantially to these burdens but remain poorly quantified globally.
Methods
We conducted an ecological country-level cross-sectional study using data from the Global Burden of Disease 2021 database, World Bank Open Data, and Our World in Data, covering 169 countries and territories. Primary outcomes were changes in age-standardized incidence rates (ASIRs) of anxiety and depressive disorders between 2019 and 2020. Exposures included changes in unemployment rates and the government stringency index (GSI) during the same period. Associations were examined overall and stratified by sex, age, and sociodemographic index (SDI).
Results
Globally, ASIRs of anxiety and depressive disorders increased in 2020 compared with 2019. Median increases were larger in high- than low-SDI countries for anxiety (17.12% vs. 11.2%) and depressive disorders (17.04% vs. 9.04%). Greater increases in unemployment were associated with larger increases in ASIR of anxiety (β = 1.43, 95% CI: 0.56–2.29) and depressive disorders (β = 1.70, 95% CI: 0.78–2.62). Higher GSI was also positively associated with increases in ASIR of anxiety (β = 1.08, 95% CI: 0.19–1.98) and depressive disorders (β = 1.34, 95% CI: 0.41–2.28). Associations were stronger in females than males and most pronounced in children and adolescents.
Conclusion
Rising unemployment and stringent government responses were significantly associated with the global increase in anxiety and depressive disorders during the COVID-19 pandemic, highlighting the need for future public health strategies that balance infection control with economic protections and mental health support
{"title":"Association of Unemployment and Government Stringency With the Increased Burden of Anxiety and Depression Amid the Public Health Emergency: A Global Perspective","authors":"Chen Zhao, Xīn Gào, Mengdi Zhang, Weihua Yue, Xiao Zhang","doi":"10.1002/brb3.71132","DOIUrl":"10.1002/brb3.71132","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The COVID-19 pandemic has coincided with marked increases in anxiety and depressive disorders. Beyond infection risks, socioeconomic stressors such as rising unemployment and stringent government responses may have contributed substantially to these burdens but remain poorly quantified globally.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted an ecological country-level cross-sectional study using data from the Global Burden of Disease 2021 database, World Bank Open Data, and Our World in Data, covering 169 countries and territories. Primary outcomes were changes in age-standardized incidence rates (ASIRs) of anxiety and depressive disorders between 2019 and 2020. Exposures included changes in unemployment rates and the government stringency index (GSI) during the same period. Associations were examined overall and stratified by sex, age, and sociodemographic index (SDI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Globally, ASIRs of anxiety and depressive disorders increased in 2020 compared with 2019. Median increases were larger in high- than low-SDI countries for anxiety (17.12% vs. 11.2%) and depressive disorders (17.04% vs. 9.04%). Greater increases in unemployment were associated with larger increases in ASIR of anxiety (<i>β</i> = 1.43, 95% CI: 0.56–2.29) and depressive disorders (<i>β</i> = 1.70, 95% CI: 0.78–2.62). Higher GSI was also positively associated with increases in ASIR of anxiety (<i>β</i> = 1.08, 95% CI: 0.19–1.98) and depressive disorders (<i>β</i> = 1.34, 95% CI: 0.41–2.28). Associations were stronger in females than males and most pronounced in children and adolescents.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Rising unemployment and stringent government responses were significantly associated with the global increase in anxiety and depressive disorders during the COVID-19 pandemic, highlighting the need for future public health strategies that balance infection control with economic protections and mental health support</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hye Yoon Park, Jaesub Park, Daeyoung Roh, Kyungun Jhung, Jhin Goo Chang, Sunyoung Park, Jin Sun Ryu, Gangho Do, Kiwon Lee, Jin Young Park, Woo Jung Kim
<div> <section> <h3> Background</h3> <p>Despite growing interest in home-based transcranial direct current stimulation (tDCS) as a scalable treatment for depression, real-world evidence regarding its effectiveness, cognitive impact, and safety remains limited. Moreover, the optimal stimulation duration for home-based tDCS has not been clearly established. This study aimed to compare the clinical effects of two home-based tDCS protocols—one with 3 weeks of active stimulation followed by 3 weeks of sham stimulation (3WA) and another with 6 weeks of active stimulation (6WA)—in patients with major depressive disorder (MDD).</p> </section> <section> <h3> Methods</h3> <p>In this randomized controlled trial, participants diagnosed with MDD were assigned to either the 3WA or 6WA group. Depressive symptoms were measured using the Beck Depression Inventory-II (BDI) and the Montgomery–Åsberg Depression Rating Scale (MADRS). Cognitive function was assessed with the Digit Symbol Substitution Test (DSST). Adverse events were systematically monitored, and the relationship between psychotropic medication use and adverse event frequency was analyzed using logistic regression.</p> </section> <section> <h3> Results</h3> <p>Both groups showed significant improvements in depressive symptoms and cognitive performance across four assessment points (baseline, Weeks 3, 6, and 12). Linear mixed-effects models revealed a significant main effect of time for both BDI (<i>F</i> = 33.67, <i>p</i> < 0.001) and MADRS scores (<i>F</i> = 34.50, <i>p</i> < 0.001), with no significant group-by-time interaction, indicating comparable efficacy between protocols. Model-derived mean changes from baseline to Week 12 were −7.53 (95% CI −9.85 to −5.21) for BDI and −6.61 (95% CI −8.73 to −4.49) for MADRS. DSST scores also improved significantly over time (<i>F</i> = 55.8, <i>p</i> < 0.001), with a mean increase of +6.62 points (95% CI +5.17 to +8.05), again showing no significant group difference. Regarding safety, non-medicated participants reported fewer adverse events, whereas those taking tianeptine experienced significantly more side effects compared with other medication groups.</p> </section> <section> <h3> Conclusions</h3> <p>Both 3-week and 6-week active tDCS protocols were associated with improvements in depressive symptoms and cognitive function over time in this naturalistic clinical context; however, as the study did not include a sham control, these changes should be interpreted as comparative rather than causal effects. The 3- and 6-week protocols demonstrated similar
背景：尽管人们对家庭经颅直流电刺激（tDCS）作为一种可扩展的抑郁症治疗方法越来越感兴趣，但关于其有效性、认知影响和安全性的现实证据仍然有限。此外，家庭tDCS的最佳刺激持续时间尚未明确确定。本研究旨在比较两种基于家庭的tDCS方案——一种是3周主动刺激，然后是3周假刺激（3WA），另一种是6周主动刺激（6WA）——对重度抑郁症（MDD）患者的临床效果。方法：在这项随机对照试验中，诊断为重度抑郁症的参与者被分为3WA组和6WA组。采用Beck抑郁量表- ii （BDI）和Montgomery-Åsberg抑郁评定量表（MADRS）测量抑郁症状。用数字符号替代测试（DSST）评估认知功能。系统监测不良事件，采用logistic回归分析精神药物使用与不良事件发生频率的关系。结果：两组在四个评估点（基线、第3周、第6周和第12周）均表现出抑郁症状和认知表现的显著改善。线性混合效应模型显示，时间对BDI （F = 33.67, p < 0.001）和MADRS评分（F = 34.50, p < 0.001）均有显著的主效应，各组间无显著的时间交互作用，表明两种治疗方案的疗效相当。从基线到第12周，模型衍生的平均变化BDI为-7.53 (95% CI -9.85至-5.21)，MADRS为-6.61 （95% CI -8.73至-4.49）。DSST评分也随时间显著改善（F = 55.8, p < 0.001），平均增加+6.62分（95% CI +5.17 ~ +8.05），同样无显著组间差异。在安全性方面，未服用药物的参与者报告的不良事件较少，而服用天奈肽的参与者与其他药物组相比，副作用明显更多。结论：在这种自然的临床背景下，3周和6周的主动tDCS方案都与抑郁症状和认知功能的改善有关；然而，由于该研究不包括假对照，这些变化应该被解释为比较效应而不是因果效应。3周和6周的治疗方案显示出相似的治疗结果，表明较短的疗程可能就足够了。这些发现支持了家庭tDCS在现实世界中的适用性，并强调了在评估耐受性和安全性时考虑同步药物治疗的必要性。试验注册：ClinicalTrials.gov标识符：NCT05539131。
{"title":"Real-World Effects of Home-Based Transcranial Direct Current Stimulation in Depression: A Randomized Controlled Trial of 3-Week Versus 6-Week Protocols","authors":"Hye Yoon Park, Jaesub Park, Daeyoung Roh, Kyungun Jhung, Jhin Goo Chang, Sunyoung Park, Jin Sun Ryu, Gangho Do, Kiwon Lee, Jin Young Park, Woo Jung Kim","doi":"10.1002/brb3.71119","DOIUrl":"10.1002/brb3.71119","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Despite growing interest in home-based transcranial direct current stimulation (tDCS) as a scalable treatment for depression, real-world evidence regarding its effectiveness, cognitive impact, and safety remains limited. Moreover, the optimal stimulation duration for home-based tDCS has not been clearly established. This study aimed to compare the clinical effects of two home-based tDCS protocols—one with 3 weeks of active stimulation followed by 3 weeks of sham stimulation (3WA) and another with 6 weeks of active stimulation (6WA)—in patients with major depressive disorder (MDD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this randomized controlled trial, participants diagnosed with MDD were assigned to either the 3WA or 6WA group. Depressive symptoms were measured using the Beck Depression Inventory-II (BDI) and the Montgomery–Åsberg Depression Rating Scale (MADRS). Cognitive function was assessed with the Digit Symbol Substitution Test (DSST). Adverse events were systematically monitored, and the relationship between psychotropic medication use and adverse event frequency was analyzed using logistic regression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Both groups showed significant improvements in depressive symptoms and cognitive performance across four assessment points (baseline, Weeks 3, 6, and 12). Linear mixed-effects models revealed a significant main effect of time for both BDI (<i>F</i> = 33.67, <i>p</i> < 0.001) and MADRS scores (<i>F</i> = 34.50, <i>p</i> < 0.001), with no significant group-by-time interaction, indicating comparable efficacy between protocols. Model-derived mean changes from baseline to Week 12 were −7.53 (95% CI −9.85 to −5.21) for BDI and −6.61 (95% CI −8.73 to −4.49) for MADRS. DSST scores also improved significantly over time (<i>F</i> = 55.8, <i>p</i> < 0.001), with a mean increase of +6.62 points (95% CI +5.17 to +8.05), again showing no significant group difference. Regarding safety, non-medicated participants reported fewer adverse events, whereas those taking tianeptine experienced significantly more side effects compared with other medication groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Both 3-week and 6-week active tDCS protocols were associated with improvements in depressive symptoms and cognitive function over time in this naturalistic clinical context; however, as the study did not include a sham control, these changes should be interpreted as comparative rather than causal effects. The 3- and 6-week protocols demonstrated similar ","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71119","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research has documented a high prevalence of cognitive and affective impairments in individuals with spinal cord injury (SCI). However, the molecular mechanisms underlying these deficits remain poorly understood. In this study, to investigate the molecular basis of cognitive and affective dysfunctions following SCI, we examined the role of calcium/calmodulin-dependent kinase II (CaMKII) activation, with a specific focus on its phosphorylated form (pCaMKII), using a rat model of SCI.
Method
Experimental results demonstrated that SCI led to spatial memory deficits as well as depression- and anxiety-like behaviors, as evidenced by performance in the Morris water maze (MWM), elevated plus maze (EPM), and forced swim test (FST). Compared to the sham group, increased levels of pCaMKII were observed in the medial prefrontal cortex (mPFC) at Day 56 after SCI. Moreover, inhibiting CaMKII phosphorylation via microinjection of KN-93—a CaMKII activation inhibitor—into the mPFC alleviated depression-like behavior and cognitive deficits, but not anxiety-like behavior.
Finds and Conclusion
These findings suggest that CaMKII activation in the mPFC may play an important role in mediating negative emotional states following SCI.
{"title":"Activation of Calcium/Calmodulin-Dependent Kinase II in the Medial Prefrontal Cortex Mediates Spinal Cord Injury-Related Cognitive and Affective Changes","authors":"Jian Qi, Chen Chen, Qian Gao, Sheng Sun","doi":"10.1002/brb3.71118","DOIUrl":"10.1002/brb3.71118","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>Research has documented a high prevalence of cognitive and affective impairments in individuals with spinal cord injury (SCI). However, the molecular mechanisms underlying these deficits remain poorly understood. In this study, to investigate the molecular basis of cognitive and affective dysfunctions following SCI, we examined the role of calcium/calmodulin-dependent kinase II (CaMKII) activation, with a specific focus on its phosphorylated form (pCaMKII), using a rat model of SCI.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>Experimental results demonstrated that SCI led to spatial memory deficits as well as depression- and anxiety-like behaviors, as evidenced by performance in the Morris water maze (MWM), elevated plus maze (EPM), and forced swim test (FST). Compared to the sham group, increased levels of pCaMKII were observed in the medial prefrontal cortex (mPFC) at Day 56 after SCI. Moreover, inhibiting CaMKII phosphorylation via microinjection of KN-93—a CaMKII activation inhibitor—into the mPFC alleviated depression-like behavior and cognitive deficits, but not anxiety-like behavior.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Finds and Conclusion</h3>\u0000 \u0000 <p>These findings suggest that CaMKII activation in the mPFC may play an important role in mediating negative emotional states following SCI.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<div> <section> <h3> Background and Aim</h3> <p>The FT4/FT3 ratio reflects thyroid hormone metabolism and has emerged as a prognostic marker in cardiovascular diseases. However, its role in ischemic stroke (IS) remains unclear. This study aimed to investigate the association between the FT4/FT3 ratio and 3-month functional outcomes in IS patients.</p> </section> <section> <h3> Methods</h3> <p>We conducted a retrospective cohort study of 199 first-episode IS patients admitted within 14 days of onset between June 2021 and June 2023. Serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were evaluated upon admission. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) at admission. Functional outcomes were evaluated using the modified Rankin Scale (mRS) at 3 months post-stroke. Poor outcome was defined as an mRS score of 3–5. Separate analyses were conducted according to FT4/FT3 ratio and outcome.</p> </section> <section> <h3> Results</h3> <p>Patients were stratified by median FT4/FT3 ratio (3.75) into low (≤ 3.75, <i>n</i> = 100) and high (> 3.75, <i>n</i> = 99) ratio groups. The high-ratio group had lower FT3 (4.14 ± 0.52 vs. 4.68 ± 0.52 pg/mL, <i>p</i> < 0.001), higher FT4 (17.83 ± 2.10 vs. 15.36 ± 1.69 pmol/L, <i>p</i> < 0.001), more diabetes (52.5% vs. 34%, <i>p</i> = 0.010), and higher proportion of poor outcomes (46.5% vs. 28%, <i>p</i> = 0.007). Receiver operating characteristic (ROC) analysis revealed that the FT4/FT3 ratio demonstrated the highest predictive ability (area under the curve [AUC] = 0.662) with an optimal cut-off of 3.845. After adjusting for NIHSS scores, age, sex, and vascular risks, the FT4/FT3 ratio remained an independent predictor of poor outcomes (odds ratio [OR] = 2.589, 95% confidence interval [CI]: 1.171 − 5.727, <i>p</i> = 0.019). FT4 was a risk factor (OR = 1.324, 95% CI: 1.045 − 1.678, <i>p</i> = 0.020), while FT3 showed a nonsignificant protective trend (OR = 0.551, 95% CI: 0.218 − 1.390, <i>p</i> = 0.207).</p> </section> <section> <h3> Conclusion</h3> <p>An elevated FT4/FT3 ratio may serve as a novel biomarker for predicting poor outcomes in ischemic stroke, reflecting thyroid hormone metabolic dysfunction that potentially exacerbates inflammation and impairs neuronal repair.</p> </section> <section> <h3> Limitations</h3> <p>This study is limited by its small sample size, single-center design, and absence of serial hormon
{"title":"The Association Between FT4/FT3 Ratio and Prognosis in Ischemic Stroke: A Retrospective Cohort Study","authors":"Guiling Wan, Linhong Mo","doi":"10.1002/brb3.71128","DOIUrl":"10.1002/brb3.71128","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aim</h3>\u0000 \u0000 <p>The FT4/FT3 ratio reflects thyroid hormone metabolism and has emerged as a prognostic marker in cardiovascular diseases. However, its role in ischemic stroke (IS) remains unclear. This study aimed to investigate the association between the FT4/FT3 ratio and 3-month functional outcomes in IS patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a retrospective cohort study of 199 first-episode IS patients admitted within 14 days of onset between June 2021 and June 2023. Serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were evaluated upon admission. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) at admission. Functional outcomes were evaluated using the modified Rankin Scale (mRS) at 3 months post-stroke. Poor outcome was defined as an mRS score of 3–5. Separate analyses were conducted according to FT4/FT3 ratio and outcome.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Patients were stratified by median FT4/FT3 ratio (3.75) into low (≤ 3.75, <i>n</i> = 100) and high (> 3.75, <i>n</i> = 99) ratio groups. The high-ratio group had lower FT3 (4.14 ± 0.52 vs. 4.68 ± 0.52 pg/mL, <i>p</i> < 0.001), higher FT4 (17.83 ± 2.10 vs. 15.36 ± 1.69 pmol/L, <i>p</i> < 0.001), more diabetes (52.5% vs. 34%, <i>p</i> = 0.010), and higher proportion of poor outcomes (46.5% vs. 28%, <i>p</i> = 0.007). Receiver operating characteristic (ROC) analysis revealed that the FT4/FT3 ratio demonstrated the highest predictive ability (area under the curve [AUC] = 0.662) with an optimal cut-off of 3.845. After adjusting for NIHSS scores, age, sex, and vascular risks, the FT4/FT3 ratio remained an independent predictor of poor outcomes (odds ratio [OR] = 2.589, 95% confidence interval [CI]: 1.171 − 5.727, <i>p</i> = 0.019). FT4 was a risk factor (OR = 1.324, 95% CI: 1.045 − 1.678, <i>p</i> = 0.020), while FT3 showed a nonsignificant protective trend (OR = 0.551, 95% CI: 0.218 − 1.390, <i>p</i> = 0.207).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>An elevated FT4/FT3 ratio may serve as a novel biomarker for predicting poor outcomes in ischemic stroke, reflecting thyroid hormone metabolic dysfunction that potentially exacerbates inflammation and impairs neuronal repair.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Limitations</h3>\u0000 \u0000 <p>This study is limited by its small sample size, single-center design, and absence of serial hormon","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/brb3.71128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Poststroke cognitive impairment (PSCI) is a common functional disorder that occurs following stroke, but there are few effective therapies. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulatory technique that has been used to improve cognitive function in stroke patients. Despite its widespread use in clinical research, the underlying mechanisms of rTMS are largely unknown. This study hypothesized that rTMS ameliorates PSCI by regulating white matter injury, which is of vital importance in cerebral ischemia.
Method
An ischemic stroke rat model was created using transient middle cerebral artery occlusion. The extents of brain damage and white matter injury, including diffusion tensor imaging and diffusion tensor tractography, were evaluated using MRI. Behavioral tests, including the modified neurological severity score test and Morris water maze test, were also used. In addition, we preliminarily explored the potential role of SDF-1α/CXCR4 by Western blot analysis and real-time reverse transcription PCR.
Finding
The results showed that 10 Hz rTMS promoted neurological recovery and cognitive deficits in ischemic rats. Additionally, 10 Hz rTMS alleviated cerebral infarct severity and attenuated white matter lesions. Furthermore, the expression levels of components of the SDF-1α/CXCR4 axis influenced the effect of rTMS on ischemic stroke.
Conclusion
This research provides further evidence that 10 Hz rTMS can alleviate white matter injury in affected brain regions and improve PSCI after ischemic stroke, potentially through the activation of the SDF-1α/CXCR4 axis.
{"title":"Repetitive Transcranial Magnetic Stimulation Improves Cognitive Impairment via the Regulation of White Matter Injury in Rats With Ischemic Stroke","authors":"Xiaoxia Hao, Qian Li, Can Luo, Xiangyu Tang, Haoyue Shao, Feng Guo","doi":"10.1002/brb3.71117","DOIUrl":"10.1002/brb3.71117","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>Poststroke cognitive impairment (PSCI) is a common functional disorder that occurs following stroke, but there are few effective therapies. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulatory technique that has been used to improve cognitive function in stroke patients. Despite its widespread use in clinical research, the underlying mechanisms of rTMS are largely unknown. This study hypothesized that rTMS ameliorates PSCI by regulating white matter injury, which is of vital importance in cerebral ischemia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>An ischemic stroke rat model was created using transient middle cerebral artery occlusion. The extents of brain damage and white matter injury, including diffusion tensor imaging and diffusion tensor tractography, were evaluated using MRI. Behavioral tests, including the modified neurological severity score test and Morris water maze test, were also used. In addition, we preliminarily explored the potential role of SDF-1α/CXCR4 by Western blot analysis and real-time reverse transcription PCR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Finding</h3>\u0000 \u0000 <p>The results showed that 10 Hz rTMS promoted neurological recovery and cognitive deficits in ischemic rats. Additionally, 10 Hz rTMS alleviated cerebral infarct severity and attenuated white matter lesions. Furthermore, the expression levels of components of the SDF-1α/CXCR4 axis influenced the effect of rTMS on ischemic stroke.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This research provides further evidence that 10 Hz rTMS can alleviate white matter injury in affected brain regions and improve PSCI after ischemic stroke, potentially through the activation of the SDF-1α/CXCR4 axis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9081,"journal":{"name":"Brain and Behavior","volume":"15 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12682929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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