Pub Date : 2025-02-05DOI: 10.1016/j.neubiorev.2025.106052
Zhengyang Wang , Yajie Xiang , Ruozhi Dang , Peng Wang , Xiaoyan Du , Peng Xie
To explore the sex-specific peripheral blood metabolites and biological functions altered in patients with major depressive disorder (MDD). A search was conducted on PubMed, Cochrane, Embase, Web of Science, and other databases published up to 11/2023. To maximize the search, we also reviewed systematic reviews and meta-analyses on the same topic. We included studies that conducted metabolic characterizations during current depressive episodes or after antidepressant treatments, with all data stratified by sex. Fifty-eight studies involving 83 cohorts with 5285 MDD participants were included in this meta-analysis. Random effects meta-analysis was conducted for data from ≥3 cohorts. We identified 5 sex-specific metabolites from 22 candidate peripheral blood metabolites. In males with MDD, we observed lower levels of estradiol and progesterone, alongside higher levels of androstenedione, dihydrotestosterone, and uric acid compared with female MDD patients. In addition, steroid hormone biosynthesis has been identified as a potentially sex-specific pathway. Our findings highlight significant evidence for targeting sex hormones as a broad understanding of MDD, providing potentially objective diagnostic and therapeutic insights.
{"title":"Sex-specific differences in peripheral blood metabolites and biological functions in major depressive disorder: A systematic review and meta-analysis","authors":"Zhengyang Wang , Yajie Xiang , Ruozhi Dang , Peng Wang , Xiaoyan Du , Peng Xie","doi":"10.1016/j.neubiorev.2025.106052","DOIUrl":"10.1016/j.neubiorev.2025.106052","url":null,"abstract":"<div><div>To explore the sex-specific peripheral blood metabolites and biological functions altered in patients with major depressive disorder (MDD). A search was conducted on PubMed, Cochrane, Embase, Web of Science, and other databases published up to 11/2023. To maximize the search, we also reviewed systematic reviews and meta-analyses on the same topic. We included studies that conducted metabolic characterizations during current depressive episodes or after antidepressant treatments, with all data stratified by sex. Fifty-eight studies involving 83 cohorts with 5285 MDD participants were included in this meta-analysis. Random effects meta-analysis was conducted for data from ≥3 cohorts. We identified 5 sex-specific metabolites from 22 candidate peripheral blood metabolites. In males with MDD, we observed lower levels of estradiol and progesterone, alongside higher levels of androstenedione, dihydrotestosterone, and uric acid compared with female MDD patients. In addition, steroid hormone biosynthesis has been identified as a potentially sex-specific pathway. Our findings highlight significant evidence for targeting sex hormones as a broad understanding of MDD, providing potentially objective diagnostic and therapeutic insights.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"170 ","pages":"Article 106052"},"PeriodicalIF":7.5,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349194","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 : 2025-02-04DOI: 10.1016/j.neubiorev.2025.106039
Sanja Mikulovic , Constanze Lenschow
Social interactions are vital for various taxa and species. Prosocial and affiliative dynamics within a group and between individuals are not only pleasurable and rewarding, but also appear to actively contribute to well-being, cognitive performance, and disease prevention. Moreover, disturbances in acting or being prosocial can represent a major burden for an individual and their affective partners. These disruptions are evident across a spectrum of neuropsychiatric conditions, including depression and autism spectrum disorders. Importantly, interactive patterns of prosocial and affiliative behavior can vary with sex. The fact that genders are differentially affected by neuropsychiatric disorders associated with social impairment underscores the high importance of this research in uncovering the underlying neural correlates and mechanisms. This review focuses on elucidating sex-related differences in prosocial and affiliative behaviors and their potential association with sexually different neural correlates. Specifically, we aim to shed light on the complex interplay between sex, behavior, and neurobiology in affiliative and prosocial interaction patterns.
{"title":"Neural control of sex differences in affiliative and prosocial behaviors","authors":"Sanja Mikulovic , Constanze Lenschow","doi":"10.1016/j.neubiorev.2025.106039","DOIUrl":"10.1016/j.neubiorev.2025.106039","url":null,"abstract":"<div><div>Social interactions are vital for various taxa and species. Prosocial and affiliative dynamics within a group and between individuals are not only pleasurable and rewarding, but also appear to actively contribute to well-being, cognitive performance, and disease prevention. Moreover, disturbances in acting or being prosocial can represent a major burden for an individual and their affective partners. These disruptions are evident across a spectrum of neuropsychiatric conditions, including depression and autism spectrum disorders. Importantly, interactive patterns of prosocial and affiliative behavior can vary with sex. The fact that genders are differentially affected by neuropsychiatric disorders associated with social impairment underscores the high importance of this research in uncovering the underlying neural correlates and mechanisms. This review focuses on elucidating sex-related differences in prosocial and affiliative behaviors and their potential association with sexually different neural correlates. Specifically, we aim to shed light on the complex interplay between sex, behavior, and neurobiology in affiliative and prosocial interaction patterns.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"171 ","pages":"Article 106039"},"PeriodicalIF":7.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366916","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 : 2025-02-04DOI: 10.1016/j.neubiorev.2025.106044
Fan Geng, Na Zhao, Qingguo Ren
Microglia, the brain's resident macrophages, are key mediators of neuroinflammation, responding to immune pathogens and toxins. They play a crucial role in clearing cellular debris, regulating synaptic plasticity, and phagocytosing amyloid-β (Aβ) plaques in Alzheimer's disease (AD). Recent studies indicate that microglia not only exhibit intrinsic circadian rhythms but are also regulated by circadian clock genes, influencing specific functions such as phagocytosis and the modulation of neuroinflammation. Disruption of the circadian rhythm is closely associated with AD pathology. In this review, we will provide an overview of how circadian rhythms regulate microglia-mediated neuroinflammation in the progression of AD, focusing on the pathway from the central nervous system (CNS) and the peripheral immune system. We also discuss potential therapeutic targets, including hormone modulation, lifestyle interventions, and anti-inflammatory therapies, aimed at maintaining brain health in AD. This will shed light on the involvement of circadian rhythm in AD and explore new avenues for AD treatment.
{"title":"Circadian rhythm, microglia-mediated neuroinflammation, and Alzheimer’s disease","authors":"Fan Geng, Na Zhao, Qingguo Ren","doi":"10.1016/j.neubiorev.2025.106044","DOIUrl":"10.1016/j.neubiorev.2025.106044","url":null,"abstract":"<div><div>Microglia, the brain's resident macrophages, are key mediators of neuroinflammation, responding to immune pathogens and toxins. They play a crucial role in clearing cellular debris, regulating synaptic plasticity, and phagocytosing amyloid-β (Aβ) plaques in Alzheimer's disease (AD). Recent studies indicate that microglia not only exhibit intrinsic circadian rhythms but are also regulated by circadian clock genes, influencing specific functions such as phagocytosis and the modulation of neuroinflammation. Disruption of the circadian rhythm is closely associated with AD pathology. In this review, we will provide an overview of how circadian rhythms regulate microglia-mediated neuroinflammation in the progression of AD, focusing on the pathway from the central nervous system (CNS) and the peripheral immune system. We also discuss potential therapeutic targets, including hormone modulation, lifestyle interventions, and anti-inflammatory therapies, aimed at maintaining brain health in AD. This will shed light on the involvement of circadian rhythm in AD and explore new avenues for AD treatment.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"170 ","pages":"Article 106044"},"PeriodicalIF":7.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143201267","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 : 2025-02-04DOI: 10.1016/j.neubiorev.2025.106042
Madeline V. Stein , Monika Heller , Natasha Hughes , Danielle Marr , Benjamin Brake , Sarah Chapman , G. James Rubin , Devin B. Terhune
Nocebo effects are a heterogenous phenomenon in which contextual cues trigger or exacerbate symptoms independently of active interventions. Suggestion, conditioning, and social observation are widely recognised as hallmark methods for inducing nocebo effects, but the extent to which nocebo effects are differentially influenced by suggestion type (e.g., direct or indirect suggestion) and mode of administration (e.g., verbal, textual, visual, etc.) across symptom domains remains unknown. We conducted a pre-registered meta-analysis (PROSPERO registration number CRD42023402097) to quantitatively synthesize available research on the factors that moderate effects in controlled nocebo experiments. Of 8469 search results, 105 experiments comprising 5017 participants and 391 effect sizes were analyzed. A multi-level meta-analysis revealed an overall moderate effect size for nocebo effects, g=0.50, [0.39, 0.62]. The magnitude of symptom expectancy effects was a significant moderator of nocebo effects. Verbal suggestion and social observation yielded moderate and comparable nocebo effects whereas technological devices, sham stimulation, and conditioning were independently associated with the induction of large nocebo effects. Greater specificity in the reporting of nocebo induction methods is required to elucidate the efficacy of different types of suggestions in inducing nocebo effects.
{"title":"Moderators of nocebo effects in controlled experiments: A multi-level meta-analysis","authors":"Madeline V. Stein , Monika Heller , Natasha Hughes , Danielle Marr , Benjamin Brake , Sarah Chapman , G. James Rubin , Devin B. Terhune","doi":"10.1016/j.neubiorev.2025.106042","DOIUrl":"10.1016/j.neubiorev.2025.106042","url":null,"abstract":"<div><div>Nocebo effects are a heterogenous phenomenon in which contextual cues trigger or exacerbate symptoms independently of active interventions. Suggestion, conditioning, and social observation are widely recognised as hallmark methods for inducing nocebo effects, but the extent to which nocebo effects are differentially influenced by suggestion type (e.g., direct or indirect suggestion) and mode of administration (e.g., verbal, textual, visual, etc.) across symptom domains remains unknown. We conducted a pre-registered meta-analysis (PROSPERO registration number CRD42023402097) to quantitatively synthesize available research on the factors that moderate effects in controlled nocebo experiments. Of 8469 search results, 105 experiments comprising 5017 participants and 391 effect sizes were analyzed. A multi-level meta-analysis revealed an overall moderate effect size for nocebo effects, <em>g</em>=0.50, [0.39, 0.62]. The magnitude of symptom expectancy effects was a significant moderator of nocebo effects. Verbal suggestion and social observation yielded moderate and comparable nocebo effects whereas technological devices, sham stimulation, and conditioning were independently associated with the induction of large nocebo effects. Greater specificity in the reporting of nocebo induction methods is required to elucidate the efficacy of different types of suggestions in inducing nocebo effects.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"172 ","pages":"Article 106042"},"PeriodicalIF":7.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366913","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 : 2025-02-03DOI: 10.1016/j.neubiorev.2025.106040
Katja Langer, Oliver T. Wolf, Christian J. Merz, Valerie L. Jentsch
The experience of stress and the need to regulate emotions are pervasive in everyday life. Emotion regulation (ER) is particularly required under stress to facilitate successful adaptation and recovery. Importantly, a growing body of work has identified stress and ER deficits as transdiagnostic risk factors for psychopathology. This highlights the relevance of understanding how stress impacts ER to elucidate individual vulnerability to mental disorders. Stress alters cognitive and emotional functioning via stress hormones secreted by the two major stress systems: sympathetic nervous system and hypothalamus-pituitary adrenocortical axis. This review aims to compile and synthesize empirical studies in humans investigating the effects of acute stress and stress hormones on ER. A systematic literature search yielded 14 relevant studies, 11 investigating acute stress effects and 3 examining the influence of pharmacological cortisol elevations on ER. The results of the stress studies are mixed revealing either impairing, beneficial or no effects at all. Cortisol administration mostly facilitated ER attempts. Notably, we detected timing differences in measuring ER performance relative to stress exposure that potentially reconcile divergent findings. Here, we propose the PRESSURE model (Predominant Stress System Underpins Regulation of Emotions) postulating that the direction and magnitude of stress effects on ER depends on the relative predominance of one stress system over the other. Additionally, sex-stress hormone interactions, stimulus intensity and ER strategy are discussed as possible moderators. Finally, we highlight limitations in current research and provide recommendations for future studies that will further advance our understanding of the intricate relationship between stress and ER.
{"title":"The effects of stress hormones on cognitive emotion regulation: A systematic review and integrative model","authors":"Katja Langer, Oliver T. Wolf, Christian J. Merz, Valerie L. Jentsch","doi":"10.1016/j.neubiorev.2025.106040","DOIUrl":"10.1016/j.neubiorev.2025.106040","url":null,"abstract":"<div><div>The experience of stress and the need to regulate emotions are pervasive in everyday life. Emotion regulation (ER) is particularly required under stress to facilitate successful adaptation and recovery. Importantly, a growing body of work has identified stress and ER deficits as transdiagnostic risk factors for psychopathology. This highlights the relevance of understanding how stress impacts ER to elucidate individual vulnerability to mental disorders. Stress alters cognitive and emotional functioning via stress hormones secreted by the two major stress systems: sympathetic nervous system and hypothalamus-pituitary adrenocortical axis. This review aims to compile and synthesize empirical studies in humans investigating the effects of acute stress and stress hormones on ER. A systematic literature search yielded 14 relevant studies, 11 investigating acute stress effects and 3 examining the influence of pharmacological cortisol elevations on ER. The results of the stress studies are mixed revealing either impairing, beneficial or no effects at all. Cortisol administration mostly facilitated ER attempts. Notably, we detected timing differences in measuring ER performance relative to stress exposure that potentially reconcile divergent findings. Here, we propose the <strong>PRESSURE</strong> model (<em><strong>Pre</strong>dominant <strong>S</strong>tress <strong>S</strong>ystem <strong>U</strong>nderpins <strong>R</strong>egulation of <strong>E</strong>motions</em>) postulating that the direction and magnitude of stress effects on ER depends on the relative predominance of one stress system over the other. Additionally, sex-stress hormone interactions, stimulus intensity and ER strategy are discussed as possible moderators. Finally, we highlight limitations in current research and provide recommendations for future studies that will further advance our understanding of the intricate relationship between stress and ER.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"170 ","pages":"Article 106040"},"PeriodicalIF":7.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257402","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.2024.105969
Pulak R. Manna , Shengping Yang , Chayan Manna , Hope Waters , Md Ariful Islam , Arubala P. Reddy , Priyanka Rawat , P. Hemachandra Reddy
The steroidogenic acute regulatory (StAR) protein mediates the rate-liming step in neuro/steroid biosynthesis. Multifaceted and delicate changes during aging, disrupting hormonal and neuronal homeostasis, constitute human senescence, an inevitable phenomenon that attributes to increased morbidity and mortality. Aging, along with progressive decreases in bioactive neurosteroids, is the primary risk factor for Alzheimer’s disease (AD), which preferentially impacts two-thirds of women and one-third of men. AD is neuropathologically characterized by the accumulation of extracellular amyloid-β and intracellular phosphorylated Tau containing neurofibrillary tangles, resulting in dementia. Postmortem brains pertaining to gender-specific AD patients exhibit varied suppression of StAR and sex neurosteroid levels compared with age-matched cognitively healthy subjects, in which the attenuation of StAR is inversely correlated with the AD pathological markers. Interestingly, retinoid signaling upregulates StAR-motivated neurosteroid biosynthesis and reinstates various neurodegenerative vulnerabilities that promote AD pathogenesis. This review summarizes current understanding of StAR-driven alterations of sex neurosteroids in gender-specific AD risks and provides biochemical and molecular insights into therapeutic interventions for preventing and/or alleviating dementia for healthy aging.
{"title":"Steroidogenic acute regulatory protein mediated variations of gender-specific sex neurosteroids in Alzheimer’s disease: Relevance to hormonal and neuronal imbalance","authors":"Pulak R. Manna , Shengping Yang , Chayan Manna , Hope Waters , Md Ariful Islam , Arubala P. Reddy , Priyanka Rawat , P. Hemachandra Reddy","doi":"10.1016/j.neubiorev.2024.105969","DOIUrl":"10.1016/j.neubiorev.2024.105969","url":null,"abstract":"<div><div>The steroidogenic acute regulatory (StAR) protein mediates the rate-liming step in neuro/steroid biosynthesis. Multifaceted and delicate changes during aging, disrupting hormonal and neuronal homeostasis, constitute human senescence, an inevitable phenomenon that attributes to increased morbidity and mortality. Aging, along with progressive decreases in bioactive neurosteroids, is the primary risk factor for Alzheimer’s disease (AD), which preferentially impacts two-thirds of women and one-third of men. AD is neuropathologically characterized by the accumulation of extracellular amyloid-β and intracellular phosphorylated Tau containing neurofibrillary tangles, resulting in dementia. Postmortem brains pertaining to gender-specific AD patients exhibit varied suppression of StAR and sex neurosteroid levels compared with age-matched cognitively healthy subjects, in which the attenuation of StAR is inversely correlated with the AD pathological markers. Interestingly, retinoid signaling upregulates StAR-motivated neurosteroid biosynthesis and reinstates various neurodegenerative vulnerabilities that promote AD pathogenesis. This review summarizes current understanding of StAR-driven alterations of sex neurosteroids in gender-specific AD risks and provides biochemical and molecular insights into therapeutic interventions for preventing and/or alleviating dementia for healthy aging.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105969"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142781926","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.2024.105991
S.V. Wass, M. Perapoch Amadó, T. Northrop, I. Marriott Haresign, E.A.M. Phillips
During early life, we develop the ability to choose what we focus on and what we ignore, allowing us to regulate perception and action in complex environments. But how does this change influence how we spontaneously allocate attention to real-world objects during free behaviour? Here, in this narrative review, we examine this question by considering the time dynamics of spontaneous overt visual attention, and how these develop through early life. Even in early childhood, visual attention shifts occur both periodically and aperiodically. These reorientations become more internally controlled as development progresses. Increasingly with age, attention states also develop self-sustaining attractor dynamics, known as attention inertia, in which the longer an attention episode lasts, the more the likelihood increases of its continuing. These self-sustaining dynamics are driven by amplificatory interactions between engagement, comprehension, and distractibility. We consider why experimental measures show decline in sustained attention over time, while real-world visual attention often demonstrates the opposite pattern. Finally, we discuss multi-stable attention states, where both hypo-arousal (mind-wandering) and hyper-arousal (fragmentary attention) may also show self-sustaining attractor dynamics driven by moment-by-moment amplificatory child-environment interactions; and we consider possible applications of this work, and future directions.
{"title":"Foraging and inertia: Understanding the developmental dynamics of overt visual attention","authors":"S.V. Wass, M. Perapoch Amadó, T. Northrop, I. Marriott Haresign, E.A.M. Phillips","doi":"10.1016/j.neubiorev.2024.105991","DOIUrl":"10.1016/j.neubiorev.2024.105991","url":null,"abstract":"<div><div>During early life, we develop the ability to choose what we focus on and what we ignore, allowing us to regulate perception and action in complex environments. But how does this change influence how we spontaneously allocate attention to real-world objects during free behaviour? Here, in this narrative review, we examine this question by considering the time dynamics of spontaneous overt visual attention, and how these develop through early life. Even in early childhood, visual attention shifts occur both periodically and aperiodically. These reorientations become more internally controlled as development progresses. Increasingly with age, attention states also develop self-sustaining attractor dynamics, known as attention inertia, in which the longer an attention episode lasts, the more the likelihood increases of its continuing. These self-sustaining dynamics are driven by amplificatory interactions between engagement, comprehension, and distractibility. We consider why experimental measures show decline in sustained attention over time, while real-world visual attention often demonstrates the opposite pattern. Finally, we discuss multi-stable attention states, where both hypo-arousal (mind-wandering) and hyper-arousal (fragmentary attention) may also show self-sustaining attractor dynamics driven by moment-by-moment amplificatory child-environment interactions; and we consider possible applications of this work, and future directions.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105991"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900604","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.2024.105980
Sarah Kappel , Sarah Collins , Michael Mendl , Carole Fureix
Understanding animal emotional (affective) state is highly relevant to various disciplines (e.g., animal welfare, neuroscience, comparative psychology), and has been significantly advanced by translating affect-induced cognitive bias paradigms rooted in human psychology to non-human animal studies. Attention bias (i.e., preferential attention allocation, AB) tests are increasingly used as more practical substitutes to commonly used judgement bias tests. Yet, evidence that AB reflects affective valence in animals is still limited. We review in-depth the concept of attention and AB described in humans and discuss utilising human-derived AB paradigms for measuring animal affective states. We describe key concepts and functions of attention in humans, before concentrating on the relationship between AB to threat detection and human anxiety. We critically review animal AB studies, discuss methodological discrepancies in such studies, and highlight the need for further experimental refinements. This includes identifying appropriate species-specific test designs and stimuli, modes of presentation (e.g., real-life vs. artificial stimuli), and consideration of subject-related factors (e.g., personality, age). We conclude that experimental limitations currently hamper the validity of AB as a proxy of animal affect and hope that the knowledge gaps highlighted in our review will encourage further research.
了解动物的情绪(情感)状态与各学科(如动物福利、神经科学、比较心理学)密切相关,通过将植根于人类心理学的情感诱导认知偏差范式转化为非人类动物研究,动物的情绪(情感)状态得到了极大的改善。注意力偏差(即优先注意力分配,AB)测试越来越多地被用来替代常用的判断偏差测试。然而,AB 反映动物情感价位的证据仍然有限。我们深入回顾了人类的注意和AB概念,并讨论了如何利用源自人类的AB范式来测量动物的情感状态。在集中讨论 AB 与威胁检测和人类焦虑之间的关系之前,我们描述了人类注意力的关键概念和功能。我们认真回顾了动物 AB 研究,讨论了此类研究在方法上的差异,并强调了进一步完善实验的必要性。这包括确定适当的特定物种测试设计和刺激物、呈现模式(如真实生活与人工刺激物),以及考虑受试者相关因素(如性格、年龄)。我们的结论是,实验的局限性目前阻碍了 AB 作为动物情感替代物的有效性,希望我们在综述中强调的知识差距能鼓励进一步的研究。
{"title":"Looking out for danger: Theoretical and empirical issues in translating human attention bias tasks to assess animal affective states","authors":"Sarah Kappel , Sarah Collins , Michael Mendl , Carole Fureix","doi":"10.1016/j.neubiorev.2024.105980","DOIUrl":"10.1016/j.neubiorev.2024.105980","url":null,"abstract":"<div><div>Understanding animal emotional (affective) state is highly relevant to various disciplines (<em>e.g.,</em> animal welfare, neuroscience, comparative psychology), and has been significantly advanced by translating affect-induced cognitive bias paradigms rooted in human psychology to non-human animal studies. Attention bias (<em>i.e.,</em> preferential attention allocation, AB) tests are increasingly used as more practical substitutes to commonly used judgement bias tests. Yet, evidence that AB reflects affective valence in animals is still limited. We review in-depth the concept of attention and AB described in humans and discuss utilising human-derived AB paradigms for measuring animal affective states. We describe key concepts and functions of attention in humans, before concentrating on the relationship between AB to threat detection and human anxiety. We critically review animal AB studies, discuss methodological discrepancies in such studies, and highlight the need for further experimental refinements. This includes identifying appropriate species-specific test designs and stimuli, modes of presentation (<em>e.g.,</em> real-life vs. artificial stimuli), and consideration of subject-related factors (<em>e.g.,</em> personality, age). We conclude that experimental limitations currently hamper the validity of AB as a proxy of animal affect and hope that the knowledge gaps highlighted in our review will encourage further research.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105980"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142820167","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.2024.106000
Attila Tóth , Árpád Dobolyi
The role of prolactin in sleep regulation has been the subject of extensive research over the past 50 years, resulting in the identification of multiple, disparate functions for the hormone. Prolactin demonstrated a characteristic circadian release pattern with elevation during dark and diminution during light. High prolactin levels were linked to non-rapid eye movement sleep and electroencephalogram delta activity in humans. Conversely, hyperprolactinemia showed strong correlation with REM sleep in rodent studies. Prolactin may be implicated in the alterations in female sleep patterns observed during the reproductive cycle, it may play a role in the REM sleep enhancement following stress and in sleep-related immunological processes. In conclusion, prolactin appears to have a sleep-promoting role, particularly during the dark phase. However, it does not appear to play a central and coherent role in sleep regulation, as observed in some neuropeptides such as orexin. Conversely, its principal function may be to facilitate situational, yet adaptive, changes in sleep patterns in response to challenging physiological phases, such as those associated with stress, immunological challenges, or the reproductive cycle. Neuronal substrates for prolactin-mediated sleep effects remain unknown; however, recent rodent sleep studies may provide insights into the potential sites of these effects.
{"title":"Prolactin in sleep and EEG regulation: New mechanisms and sleep-related brain targets complement classical data","authors":"Attila Tóth , Árpád Dobolyi","doi":"10.1016/j.neubiorev.2024.106000","DOIUrl":"10.1016/j.neubiorev.2024.106000","url":null,"abstract":"<div><div>The role of prolactin in sleep regulation has been the subject of extensive research over the past 50 years, resulting in the identification of multiple, disparate functions for the hormone. Prolactin demonstrated a characteristic circadian release pattern with elevation during dark and diminution during light. High prolactin levels were linked to non-rapid eye movement sleep and electroencephalogram delta activity in humans. Conversely, hyperprolactinemia showed strong correlation with REM sleep in rodent studies. Prolactin may be implicated in the alterations in female sleep patterns observed during the reproductive cycle, it may play a role in the REM sleep enhancement following stress and in sleep-related immunological processes. In conclusion, prolactin appears to have a sleep-promoting role, particularly during the dark phase. However, it does not appear to play a central and coherent role in sleep regulation, as observed in some neuropeptides such as orexin. Conversely, its principal function may be to facilitate situational, yet adaptive, changes in sleep patterns in response to challenging physiological phases, such as those associated with stress, immunological challenges, or the reproductive cycle. Neuronal substrates for prolactin-mediated sleep effects remain unknown; however, recent rodent sleep studies may provide insights into the potential sites of these effects.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106000"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928813","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.2025.106017
Sarah Ulrich , Else Schneider , Gunnar Deuring , Saskia Erni , Magdalena Ridder , Jan Sarlon , Annette B. Brühl
Electroconvulsive therapy (ECT) is highly efficacious for the treatment of major depressive disorder (MDD), but its mechanisms still require clarification. Even though depression is associated with alterations in functional connectivity (FC), EEG studies investigating effects of ECT on FC have not been systematically reviewed. Understanding these effects may help to identify the role of functional brain circuits in depression and its remission. This systematic review aimed to synthesize EEG studies investigating FC changes in ECT-treated patients with depression. A systematic literature search was conducted following PRISMA guidelines. Peer-reviewed studies on pre-to post-ECT resting-state EEG FC changes in adult patients with MDD were included. Three of 143 studies were included, of which two reported reduced FC in the alpha and beta frequency bands and increased theta band FC in patients with ECT-treated MDD. Changes in alpha band FC were associated with treatment outcomes. Patients with MDD exhibit increased electrophysiological resting-state alpha band FC, particularly frontally, compared with healthy subjects. Thus, ECT-induced decrease might indicate a trend toward normalization of oscillatory brain rhythms. As brain oscillations have been proposed to be involved in neuronal synchronization, which is important for communication between networks, the potential restoration in patients with depression and the association of FC changes with clinical improvement may indicate a potential mechanism of action of ECT. Understanding ECT’s underlying mechanisms might ultimately enable treatment optimization, thus enhancing patient care. However, the number of studies is limited, with low-to-moderate EEG study quality, small sample sizes, and different electrophysiological FC measures.
{"title":"Alterations in resting-state EEG functional connectivity in patients with major depressive disorder receiving electroconvulsive therapy: A systematic review","authors":"Sarah Ulrich , Else Schneider , Gunnar Deuring , Saskia Erni , Magdalena Ridder , Jan Sarlon , Annette B. Brühl","doi":"10.1016/j.neubiorev.2025.106017","DOIUrl":"10.1016/j.neubiorev.2025.106017","url":null,"abstract":"<div><div>Electroconvulsive therapy (ECT) is highly efficacious for the treatment of major depressive disorder (MDD), but its mechanisms still require clarification. Even though depression is associated with alterations in functional connectivity (FC), EEG studies investigating effects of ECT on FC have not been systematically reviewed. Understanding these effects may help to identify the role of functional brain circuits in depression and its remission. This systematic review aimed to synthesize EEG studies investigating FC changes in ECT-treated patients with depression. A systematic literature search was conducted following PRISMA guidelines. Peer-reviewed studies on pre-to post-ECT resting-state EEG FC changes in adult patients with MDD were included. Three of 143 studies were included, of which two reported reduced FC in the alpha and beta frequency bands and increased theta band FC in patients with ECT-treated MDD. Changes in alpha band FC were associated with treatment outcomes. Patients with MDD exhibit increased electrophysiological resting-state alpha band FC, particularly frontally, compared with healthy subjects. Thus, ECT-induced decrease might indicate a trend toward normalization of oscillatory brain rhythms. As brain oscillations have been proposed to be involved in neuronal synchronization, which is important for communication between networks, the potential restoration in patients with depression and the association of FC changes with clinical improvement may indicate a potential mechanism of action of ECT. Understanding ECT’s underlying mechanisms might ultimately enable treatment optimization, thus enhancing patient care. However, the number of studies is limited, with low-to-moderate EEG study quality, small sample sizes, and different electrophysiological FC measures.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106017"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017088","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}