Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2024.105994
Anita Snowdon-Farrell , Chiara Attal , Naghmeh Nikkheslat , Carmine Pariante , Allan H. Young , Roland Zahn
Oxytocin was hypothesised to play a critical role in forming and maintaining secure attachments, shown to confer resilience against affective disorders. The endogenous opioid system has also emerged as a key player in attachment dynamics. In this pre-registered systematic review, we investigated whether individual differences in the functioning of these neurochemical systems are related to attachment styles, following PRISMA guidelines. As predicted, individuals with higher oxytocin function exhibited more secure attachment styles (p = .006, n = 12 studies) and less insecure attachment styles (p = .021, n = 16 studies). Contrary to our hypothesis, we found no association of endogenous opioid function with insecure (p = 0.549, n = 11 studies) or secure attachment styles (p = .065, n = 11 studies). The lack of association between endogenous mu-opioid function and attachment styles remains inconclusive due to inconsistencies in the neurochemical measurements and lack of eligible studies. Therefore, further investigations into the role of the endogenous opioid system in attachment styles are needed. Our findings corroborate the hypothesis that individual differences in oxytocin function relate to differences in attachment styles.
{"title":"How does neurochemistry affect attachment styles in humans? The role of oxytocin and the endogenous opioid system in sociotropy and autonomy – A systematic review","authors":"Anita Snowdon-Farrell , Chiara Attal , Naghmeh Nikkheslat , Carmine Pariante , Allan H. Young , Roland Zahn","doi":"10.1016/j.neubiorev.2024.105994","DOIUrl":"10.1016/j.neubiorev.2024.105994","url":null,"abstract":"<div><div>Oxytocin was hypothesised to play a critical role in forming and maintaining secure attachments, shown to confer resilience against affective disorders. The endogenous opioid system has also emerged as a key player in attachment dynamics. In this pre-registered systematic review, we investigated whether individual differences in the functioning of these neurochemical systems are related to attachment styles, following PRISMA guidelines. As predicted, individuals with higher oxytocin function exhibited more secure attachment styles (p = .006, n = 12 studies) and less insecure attachment styles (p = .021, n = 16 studies). Contrary to our hypothesis, we found no association of endogenous opioid function with insecure (p = 0.549, n = 11 studies) or secure attachment styles (p = .065, n = 11 studies). The lack of association between endogenous mu-opioid function and attachment styles remains inconclusive due to inconsistencies in the neurochemical measurements and lack of eligible studies. Therefore, further investigations into the role of the endogenous opioid system in attachment styles are needed. Our findings corroborate the hypothesis that individual differences in oxytocin function relate to differences in attachment styles.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105994"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2025.106029
Serafina Perrone , Virginia Beretta , Maria Luisa Tataranno , Sidhartha Tan , Zhongjie Shi , Elena Scarpa , Valentina Dell’Orto , Sebastiano Ravenda , Chiara Petrolini , Maria Maddalena Brambilla , Paola Palanza , Eloisa Gitto , Francesco Nonnis-Marzano
Perinatal asphyxia (PA) is a leading cause of neonatal morbidity and mortality, often resulting in long-term neurodevelopmental challenges. Despite advancements in perinatal care, predicting long-term outcomes remains difficult. Early diagnosis is essential for timely interventions to reduce brain injury, with tools such as Magnetic Resonance Imaging, brain ultrasound, and emerging biomarkers playing a possible key role. Olfaction, one of the earliest senses to develop, may provide valuable insights into long-term neurodevelopmental outcomes following PA due to its intricate neural connections with regions responsible for memory, emotion, and homeostasis. Newborns demonstrate early olfactory abilities, such as recognizing maternal odors, which are vital for bonding, feeding, and emotional regulation. These responses are processed by a network of brain regions, including the olfactory bulb (OB), piriform cortex, amygdala, and orbitofrontal cortex. Hypoxic injury to these regions, particularly the OB, may disrupt olfactory processing in infants with PA, potentially affecting their cognitive and social development. Investigating the relationship between olfactory system development and perinatal brain injury could lead to innovative diagnostic and therapeutic approaches. Further research, including clinical and animal studies, is necessary to fully explore the potential of olfactory assessments in predicting outcomes after PA. This educational review explores and discusses the potential of olfaction as a predictor of long-term outcomes and a tool for risk stratification following PA, opening new pathways for interventions and improved care.
{"title":"Olfactory testing in infants with perinatal asphyxia: Enhancing encephalopathy risk stratification for future health outcomes","authors":"Serafina Perrone , Virginia Beretta , Maria Luisa Tataranno , Sidhartha Tan , Zhongjie Shi , Elena Scarpa , Valentina Dell’Orto , Sebastiano Ravenda , Chiara Petrolini , Maria Maddalena Brambilla , Paola Palanza , Eloisa Gitto , Francesco Nonnis-Marzano","doi":"10.1016/j.neubiorev.2025.106029","DOIUrl":"10.1016/j.neubiorev.2025.106029","url":null,"abstract":"<div><div>Perinatal asphyxia (PA) is a leading cause of neonatal morbidity and mortality, often resulting in long-term neurodevelopmental challenges. Despite advancements in perinatal care, predicting long-term outcomes remains difficult. Early diagnosis is essential for timely interventions to reduce brain injury, with tools such as Magnetic Resonance Imaging, brain ultrasound, and emerging biomarkers playing a possible key role. Olfaction, one of the earliest senses to develop, may provide valuable insights into long-term neurodevelopmental outcomes following PA due to its intricate neural connections with regions responsible for memory, emotion, and homeostasis. Newborns demonstrate early olfactory abilities, such as recognizing maternal odors, which are vital for bonding, feeding, and emotional regulation. These responses are processed by a network of brain regions, including the olfactory bulb (OB), piriform cortex, amygdala, and orbitofrontal cortex. Hypoxic injury to these regions, particularly the OB, may disrupt olfactory processing in infants with PA, potentially affecting their cognitive and social development. Investigating the relationship between olfactory system development and perinatal brain injury could lead to innovative diagnostic and therapeutic approaches. Further research, including clinical and animal studies, is necessary to fully explore the potential of olfactory assessments in predicting outcomes after PA. This educational review explores and discusses the potential of olfaction as a predictor of long-term outcomes and a tool for risk stratification following PA, opening new pathways for interventions and improved care.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106029"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2024.105998
Carmen Morawetz , Florian J. Hemetsberger , Angela R. Laird , Nils Kohn
{"title":"Corrigendum to “Emotion Regulation: From neural circuits to a transdiagnostic perspective” [Neurosci. Biobehav. Rev. (2025) 168:105960]","authors":"Carmen Morawetz , Florian J. Hemetsberger , Angela R. Laird , Nils Kohn","doi":"10.1016/j.neubiorev.2024.105998","DOIUrl":"10.1016/j.neubiorev.2024.105998","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105998"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2025.106025
Geng Li , Haishuo Xia , Gesi Teng , Antao Chen
{"title":"Corrigendum to “The neural correlates of physical exercise-induced general cognitive gains: A systematic review and meta-analysis of functional magnetic resonance imaging studies” [Neurosci. Biobehav. Rev. 169 (2025) 106008]","authors":"Geng Li , Haishuo Xia , Gesi Teng , Antao Chen","doi":"10.1016/j.neubiorev.2025.106025","DOIUrl":"10.1016/j.neubiorev.2025.106025","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106025"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2024.105971
Aurélien Riou , Aline Broeglin , Amandine Grimm
Mitochondrial transplantation is a new treatment strategy aimed at repairing cellular damage by introducing healthy mitochondria into injured cells. The approach shows promise in protecting brain function in various neurological disorders such as traumatic brain injury/ischemia, neurodegenerative diseases, cognitive disorders, and cancer. These conditions are often characterized by mitochondrial dysfunction, leading to impaired energy production and neuronal death. The review highlights promising preclinical studies where mitochondrial transplantation has been shown to restore mitochondrial function, reduce inflammation, and improve cognitive and motor functions in several animal models. It also addresses significant challenges that must be overcome before this therapy can be clinically applied. Current efforts to overcome these challenges, including advancements in isolation techniques, cryopreservation methods, finding an appropriate mitochondria source, and potential delivery routes, are discussed. Considering the rising incidence of neurological disorders and the limited effectiveness of current treatments, this review offers a comprehensive overview of the current state of mitochondrial transplantation research and critically assesses the remaining obstacles. It provides valuable insights that could steer future studies and potentially lead to more effective treatments for various brain disorders.
{"title":"Mitochondrial transplantation in brain disorders: Achievements, methods, and challenges","authors":"Aurélien Riou , Aline Broeglin , Amandine Grimm","doi":"10.1016/j.neubiorev.2024.105971","DOIUrl":"10.1016/j.neubiorev.2024.105971","url":null,"abstract":"<div><div>Mitochondrial transplantation is a new treatment strategy aimed at repairing cellular damage by introducing healthy mitochondria into injured cells. The approach shows promise in protecting brain function in various neurological disorders such as traumatic brain injury/ischemia, neurodegenerative diseases, cognitive disorders, and cancer. These conditions are often characterized by mitochondrial dysfunction, leading to impaired energy production and neuronal death. The review highlights promising preclinical studies where mitochondrial transplantation has been shown to restore mitochondrial function, reduce inflammation, and improve cognitive and motor functions in several animal models. It also addresses significant challenges that must be overcome before this therapy can be clinically applied. Current efforts to overcome these challenges, including advancements in isolation techniques, cryopreservation methods, finding an appropriate mitochondria source, and potential delivery routes, are discussed. Considering the rising incidence of neurological disorders and the limited effectiveness of current treatments, this review offers a comprehensive overview of the current state of mitochondrial transplantation research and critically assesses the remaining obstacles. It provides valuable insights that could steer future studies and potentially lead to more effective treatments for various brain disorders.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105971"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142787728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2025.106005
Ketsupar Jirakran , Abbas F. Almulla , Thapanee Jaipinta , Asara Vasupanrajit , Priabprat Jansem , Chavit Tunvirachaisakul , Elizabet Dzhambazova , Drozdstoj St. Stoyanov , Michael Maes
Background
Major depressive disorder (MDD) and bipolar disorder (BD) often coexist with metabolic syndrome. Both are linked to increased atherogenicity and a higher risk of cardiovascular diseases. Nevertheless, a comprehensive analysis of key atherogenic biomarkers in MDD/BD is still lacking.
Objectives
This meta-analysis evaluates the relationship between atherogenic indices and MDD/BD, while identifying the most effective atherogenic biomarker.
Methods
This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched electronic databases, including PubMed, Google Scholar, and Web of Science, for articles published up to August 1, 2024.
Results
We included 85 eligible studies (14 on BD and 71 on MDD), covering 70,856 participants: 18,738 patients and 52,118 healthy controls. MDD/BD patients showed significant increases (p < 0.001) in the Castelli Risk Index 2 (CRI2), Atherogenic Index of Plasma (AIP), and (triglyceride or TG + low-density lipoprotein + very low-density lipoprotein)/(high-density lipoprotein cholesterol or HDL + Apolipoprotein A or ApoA) ratio, but not CRI1 and ApoB/ApoA ratio. Significant lower HDL and lecithin: cholesterol acyltransferase activity, and higher TG levels were observed in MDD/BD patients compared with controls. There were no significant differences between MDD and BD patients. Most included studies lacked the most essential information on the inclusion and exclusion of important confounders.
Conclusions
AIP is the most effective atherogenicity index for mood disorders. Regular lipid profiling and metabolic syndrome screening are crucial in MDD/BD. Early intervention with lipid-lowering therapies is recommended to prevent the worsening of atherogenicity and disease progression.
背景:重度抑郁障碍(MDD)和双相情感障碍(BD)常与代谢综合征共存。两者都与动脉粥样硬化性增加和心血管疾病风险增加有关。然而,对MDD/BD的关键动脉粥样硬化生物标志物的综合分析仍然缺乏。目的:本荟萃分析评估了动脉粥样硬化指标与MDD/BD之间的关系,同时确定了最有效的动脉粥样硬化生物标志物。方法:本研究遵循系统评价和荟萃分析指南的首选报告项目。我们检索了电子数据库,包括PubMed、b谷歌Scholar和Web of Science,检索了截止到2024年8月1日发表的文章。结果:我们纳入了85项符合条件的研究(14项双相障碍研究和71项重度抑郁症研究),涵盖70,856名参与者:18,738名患者和52,118名健康对照。MDD/BD患者的Castelli风险指数2 (CRI2)、血浆致动脉粥样硬化指数(AIP)和(甘油三酯或TG +低密度脂蛋白+极低密度脂蛋白)/(高密度脂蛋白胆固醇或HDL +载脂蛋白A或ApoA)比值显著升高(p < 0.001),但CRI1和ApoB/ApoA比值无显著升高。与对照组相比,MDD/BD患者的HDL和卵磷脂、胆固醇酰基转移酶活性显著降低,TG水平较高。MDD和BD患者之间无显著差异。大多数纳入的研究缺乏关于纳入和排除重要混杂因素的最基本信息。结论:AIP是诊断心境障碍最有效的动脉粥样硬化指数。定期的脂质分析和代谢综合征筛查对MDD/BD至关重要。建议采用降脂疗法进行早期干预,以防止动脉粥样硬化恶化和疾病进展。
{"title":"Increased atherogenicity in mood disorders: a systematic review, meta-analysis and meta-regression","authors":"Ketsupar Jirakran , Abbas F. Almulla , Thapanee Jaipinta , Asara Vasupanrajit , Priabprat Jansem , Chavit Tunvirachaisakul , Elizabet Dzhambazova , Drozdstoj St. Stoyanov , Michael Maes","doi":"10.1016/j.neubiorev.2025.106005","DOIUrl":"10.1016/j.neubiorev.2025.106005","url":null,"abstract":"<div><h3>Background</h3><div>Major depressive disorder (MDD) and bipolar disorder (BD) often coexist with metabolic syndrome. Both are linked to increased atherogenicity and a higher risk of cardiovascular diseases. Nevertheless, a comprehensive analysis of key atherogenic biomarkers in MDD/BD is still lacking.</div></div><div><h3>Objectives</h3><div>This meta-analysis evaluates the relationship between atherogenic indices and MDD/BD, while identifying the most effective atherogenic biomarker.</div></div><div><h3>Methods</h3><div>This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched electronic databases, including PubMed, Google Scholar, and Web of Science, for articles published up to August 1, 2024.</div></div><div><h3>Results</h3><div>We included 85 eligible studies (14 on BD and 71 on MDD), covering 70,856 participants: 18,738 patients and 52,118 healthy controls. MDD/BD patients showed significant increases (p < 0.001) in the Castelli Risk Index 2 (CRI2), Atherogenic Index of Plasma (AIP), and (triglyceride or TG + low-density lipoprotein + very low-density lipoprotein)/(high-density lipoprotein cholesterol or HDL + Apolipoprotein A or ApoA) ratio, but not CRI1 and ApoB/ApoA ratio. Significant lower HDL and lecithin: cholesterol acyltransferase activity, and higher TG levels were observed in MDD/BD patients compared with controls. There were no significant differences between MDD and BD patients. Most included studies lacked the most essential information on the inclusion and exclusion of important confounders.</div></div><div><h3>Conclusions</h3><div>AIP is the most effective atherogenicity index for mood disorders. Regular lipid profiling and metabolic syndrome screening are crucial in MDD/BD. Early intervention with lipid-lowering therapies is recommended to prevent the worsening of atherogenicity and disease progression.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106005"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142967447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2025.106016
Fay E. Clark
Play in humans and other animals is widespread and intuitive to recognise. Creative, unstructured play is difficult to quantify, but games direct play towards a specific goal and have defined rules, mechanics and rewards. To date, games have been under-utilised in human and animal behavioural neuroscience. This review evaluates evidence that animals can play human games, including game-theory contests, tangible games, and video games. Animals can be trained to play various human games with cognitive capacities such as role adoption, rule-following and performance monitoring. Animals can make irrational gameplay decisions that jeopardise rewards and have salient emotional responses to winning and losing. Games can advance the field of behavioural neuroscience in several ways. Cognitive tasks can become more engaging and ecologically relevant by adding game elements, known as gamification. Games can be used to induce and measure more naturalistic emotional responses to the process of overcoming (progression/regression) and end state (winning/losing) of cognitive challenges. There is also scope to target specific cognitive skill deficiencies in captive animals using games. However, a recent rapid increase in computerised testing environments raises an important ethical question about the boundary between games and reality for animals.
{"title":"Levelling up the study of animal gameplay","authors":"Fay E. Clark","doi":"10.1016/j.neubiorev.2025.106016","DOIUrl":"10.1016/j.neubiorev.2025.106016","url":null,"abstract":"<div><div>Play in humans and other animals is widespread and intuitive to recognise. Creative, unstructured play is difficult to quantify, but games direct play towards a specific goal and have defined rules, mechanics and rewards. To date, games have been under-utilised in human and animal behavioural neuroscience. This review evaluates evidence that animals can play human games, including game-theory contests, tangible games, and video games. Animals can be trained to play various human games with cognitive capacities such as role adoption, rule-following and performance monitoring. Animals can make irrational gameplay decisions that jeopardise rewards and have salient emotional responses to winning and losing. Games can advance the field of behavioural neuroscience in several ways. Cognitive tasks can become more engaging and ecologically relevant by adding game elements, known as gamification. Games can be used to induce and measure more naturalistic emotional responses to the process of overcoming (progression/regression) and end state (winning/losing) of cognitive challenges. There is also scope to target specific cognitive skill deficiencies in captive animals using games. However, a recent rapid increase in computerised testing environments raises an important ethical question about the boundary between games and reality for animals.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106016"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2025.106008
Geng Li , Haishuo Xia , Gesi Teng , Antao Chen
The general-domain effect of physical exercise-induced cognitive gains in behavioral outcomes is well-documented, but a consensus on the neural correlates remains elusive. This meta-analysis aims to identify the neural correlates of physical exercise-induced general cognitive gains by examining task-related brain activation consistently modulated by physical exercise and its relationship to those gains. Our analysis of 52 studies with 1503 participants shows that physical exercise enhances cognitive task performance (Hedges' g = 0.271) and consistently increases task-related brain activation primarily in the bilateral precuneus. These increases in task-related brain activation correlate positively with cognitive task performance improvements improvements. Notably, physical exercise intensity, adherence, and social environment significantly modulate task-related brain activation changes induced by physical exercise. This meta-analysis offers an unprecedented comprehensive assessment of how physical exercise modulates task-related brain activation changes, providing neural evidence to support the general-domain effects on cognitive function induced by physical exercise.
体育锻炼在行为结果中诱导的认知增益的一般域效应已被充分证明,但关于神经相关性的共识仍未达成。本荟萃分析旨在通过研究体育锻炼持续调节的任务相关大脑激活及其与认知能力提高的关系,确定体育锻炼诱导的一般认知能力提高的神经相关因素。我们对 52 项研究、1,503 名参与者进行的分析表明,体育锻炼可提高任务绩效(赫奇斯 g = 0.271),并持续增加与任务相关的大脑激活,主要是在双侧楔前肌。这些任务相关大脑激活的增加与任务表现的提高呈正相关。值得注意的是,体育锻炼的强度、坚持程度和社会环境会显著调节体育锻炼引起的任务相关脑激活变化。这项荟萃分析对体育锻炼如何调节与任务相关的大脑激活变化进行了前所未有的全面评估,为体育锻炼对认知功能的一般领域影响提供了神经证据。
{"title":"The neural correlates of physical exercise-induced general cognitive gains: A systematic review and meta-analysis of functional magnetic resonance imaging studies","authors":"Geng Li , Haishuo Xia , Gesi Teng , Antao Chen","doi":"10.1016/j.neubiorev.2025.106008","DOIUrl":"10.1016/j.neubiorev.2025.106008","url":null,"abstract":"<div><div>The general-domain effect of physical exercise-induced cognitive gains in behavioral outcomes is well-documented, but a consensus on the neural correlates remains elusive. This meta-analysis aims to identify the neural correlates of physical exercise-induced general cognitive gains by examining task-related brain activation consistently modulated by physical exercise and its relationship to those gains. Our analysis of 52 studies with 1503 participants shows that physical exercise enhances cognitive task performance (Hedges' <em>g</em> = 0.271) and consistently increases task-related brain activation primarily in the bilateral precuneus. These increases in task-related brain activation correlate positively with cognitive task performance improvements improvements. Notably, physical exercise intensity, adherence, and social environment significantly modulate task-related brain activation changes induced by physical exercise. This meta-analysis offers an unprecedented comprehensive assessment of how physical exercise modulates task-related brain activation changes, providing neural evidence to support the general-domain effects on cognitive function induced by physical exercise.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106008"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2024.105966
Sabrina Trapp , David Whitney , David Pascucci
Where do novel research questions come from? We suggest that identifying key computational problems and comparing solutions across domains can be one source. We exemplify this by looking at perception and action and outline how findings from one domain may generate novel research avenues in the other.
{"title":"The computational perspective: A catalyst for research questions in cognitive neuroscience?","authors":"Sabrina Trapp , David Whitney , David Pascucci","doi":"10.1016/j.neubiorev.2024.105966","DOIUrl":"10.1016/j.neubiorev.2024.105966","url":null,"abstract":"<div><div>Where do novel research questions come from? We suggest that identifying key computational problems and comparing solutions across domains can be one source. We exemplify this by looking at perception and action and outline how findings from one domain may generate novel research avenues in the other.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105966"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142774807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2025.106035
Robert Dantzer , Brandon Chelette , Elisabeth G. Vichaya , A. Phillip West , Aaron Grossberg
Although we are all familiar with the sensation of fatigue, there are still profound divergences on what it represents and its mechanisms. Fatigue can take various forms depending on the condition in which it develops. Cancer-related fatigue is considered a symptom of exhaustion that is often present at the time of diagnosis, increases in intensity during cancer therapy, and does not always recede after completion of treatment. It is usually attributed to the inflammation induced by damage-associated molecular patterns released by tumor cells during cancer progression and in response to its treatment. In this review, we argue that it is necessary to go beyond the symptoms of fatigue to understand its nature and mechanisms. We propose to consider fatigue as a psychobiological process that regulates the behavioral activities an organism engages in to satisfy its needs, according to its physical ability to do so and to the capacity of its intermediary metabolism to exploit the resources procured by these activities. This last aspect is critical as it implies that these metabolic aspects need to be considered to understand fatigue. Based on the findings we have accumulated over several years of studying fatigue in diverse murine models of cancer, we show that energy metabolism plays a key role in the development and persistence of this condition. Cancer-related fatigue is dependent on the energy requirements of the tumor and the negative impact of cancer therapy on the mitochondrial function of the host. When inflammation is present, it adds to the organism’s energy expenses. The organism needs to adjust its metabolism to the different forms of cellular stress it experiences thanks to specialized communication factors known as mitokines that act locally and at a distance from the cells in which they are produced. They induce the subjective, behavioral, and metabolic components of fatigue by acting in the brain. Therefore, the targeting of mitokines and their brain receptors offers a window of opportunity to treat fatigue when it is no longer adaptive but an obstacle to the quality of life of cancer survivors.
{"title":"The metabolic basis of cancer-related fatigue","authors":"Robert Dantzer , Brandon Chelette , Elisabeth G. Vichaya , A. Phillip West , Aaron Grossberg","doi":"10.1016/j.neubiorev.2025.106035","DOIUrl":"10.1016/j.neubiorev.2025.106035","url":null,"abstract":"<div><div>Although we are all familiar with the sensation of fatigue, there are still profound divergences on what it represents and its mechanisms. Fatigue can take various forms depending on the condition in which it develops. Cancer-related fatigue is considered a symptom of exhaustion that is often present at the time of diagnosis, increases in intensity during cancer therapy, and does not always recede after completion of treatment. It is usually attributed to the inflammation induced by damage-associated molecular patterns released by tumor cells during cancer progression and in response to its treatment. In this review, we argue that it is necessary to go beyond the symptoms of fatigue to understand its nature and mechanisms. We propose to consider fatigue as a psychobiological process that regulates the behavioral activities an organism engages in to satisfy its needs, according to its physical ability to do so and to the capacity of its intermediary metabolism to exploit the resources procured by these activities. This last aspect is critical as it implies that these metabolic aspects need to be considered to understand fatigue. Based on the findings we have accumulated over several years of studying fatigue in diverse murine models of cancer, we show that energy metabolism plays a key role in the development and persistence of this condition. Cancer-related fatigue is dependent on the energy requirements of the tumor and the negative impact of cancer therapy on the mitochondrial function of the host. When inflammation is present, it adds to the organism’s energy expenses. The organism needs to adjust its metabolism to the different forms of cellular stress it experiences thanks to specialized communication factors known as mitokines that act locally and at a distance from the cells in which they are produced. They induce the subjective, behavioral, and metabolic components of fatigue by acting in the brain. Therefore, the targeting of mitokines and their brain receptors offers a window of opportunity to treat fatigue when it is no longer adaptive but an obstacle to the quality of life of cancer survivors.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106035"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}