Pub Date : 2025-04-14DOI: 10.1016/j.neubiorev.2025.106162
Abdul Nasir , Maryam Afridi , Ome Kalsoom Afridi , Muhammad Arif Khan , Amir Khan , Jun Zhang , Bai Qian
The transition from acute to chronic pain is a complex and multifactorial process that presents significant challenges in both diagnosis and treatment. Key mechanisms of peripheral and central sensitization, neuroinflammation, and altered synaptic plasticity contribute to the amplification of pain signals and the persistence of pain. Glial cell activation, particularly microglia and astrocytes, is pivotal in developing chronic pain by releasing pro-inflammatory cytokines that enhance pain sensitivity. This review explores the molecular, cellular, and systemic mechanisms underlying the transition from acute to chronic pain, offering new insights into the molecular and neurobiological mechanisms involved, which are often underexplored in existing literature. It also addresses emerging therapeutic strategies beyond traditional pain management, offering valuable perspectives for future research and clinical applications.
{"title":"The persistent pain enigma: Molecular drivers behind acute-to-chronic transition","authors":"Abdul Nasir , Maryam Afridi , Ome Kalsoom Afridi , Muhammad Arif Khan , Amir Khan , Jun Zhang , Bai Qian","doi":"10.1016/j.neubiorev.2025.106162","DOIUrl":"10.1016/j.neubiorev.2025.106162","url":null,"abstract":"<div><div>The transition from acute to chronic pain is a complex and multifactorial process that presents significant challenges in both diagnosis and treatment. Key mechanisms of peripheral and central sensitization, neuroinflammation, and altered synaptic plasticity contribute to the amplification of pain signals and the persistence of pain. Glial cell activation, particularly microglia and astrocytes, is pivotal in developing chronic pain by releasing pro-inflammatory cytokines that enhance pain sensitivity. This review explores the molecular, cellular, and systemic mechanisms underlying the transition from acute to chronic pain, offering new insights into the molecular and neurobiological mechanisms involved, which are often underexplored in existing literature. It also addresses emerging therapeutic strategies beyond traditional pain management, offering valuable perspectives for future research and clinical applications.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106162"},"PeriodicalIF":7.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834481","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 : 2025-04-11DOI: 10.1016/j.neubiorev.2025.106143
Maarten Laroy , Louise Emsell , Mathieu Vandenbulcke , Filip Bouckaert
Since its introduction in 1938, the precise mechanism underlying the efficacy of electroconvulsive therapy (ECT) in treating severe psychiatric disorders remains elusive. This paper presents a comprehensive scoping review aimed to collate and summarize findings from clinical studies on neuroplastic changes induced by ECT. The review categorizes neuroplasticity into molecular, structural, and functional domains, offering a multilevel view of current research and its limitations. Molecular findings detail the varied responses of neurotrophic factors and neurotransmitters post-ECT, highlighting inconsistent evidence on their clinical relevance. Structural neuroplasticity is explored through changes in brain volume, cortical thickness, and white matter properties, presenting ECT as a potent stimulator of brain architecture alterations. Functional plasticity examines ECT's impact on brain function through diverse neuroimaging techniques, suggesting significant yet complex modifications in brain network connectivity and activity. The review emphasizes the multilevel nature of these neuroplasticity levels and their collective role in ECT's therapeutic outcomes. Methodological considerations—including sample size, patient heterogeneity, and variability in assessment timing—emerge as recurring themes in the literature, underscoring the need for more consistent and rigorous research designs. By outlining a cohesive framework of changes in neuroplasticity due to ECT, this review provides initial steps towards a deeper comprehension of ECT's mechanisms.
{"title":"Mapping electroconvulsive therapy induced neuroplasticity: Towards a multilevel understanding of the available clinical literature – A scoping review","authors":"Maarten Laroy , Louise Emsell , Mathieu Vandenbulcke , Filip Bouckaert","doi":"10.1016/j.neubiorev.2025.106143","DOIUrl":"10.1016/j.neubiorev.2025.106143","url":null,"abstract":"<div><div>Since its introduction in 1938, the precise mechanism underlying the efficacy of electroconvulsive therapy (ECT) in treating severe psychiatric disorders remains elusive. This paper presents a comprehensive scoping review aimed to collate and summarize findings from clinical studies on neuroplastic changes induced by ECT. The review categorizes neuroplasticity into molecular, structural, and functional domains, offering a multilevel view of current research and its limitations. Molecular findings detail the varied responses of neurotrophic factors and neurotransmitters post-ECT, highlighting inconsistent evidence on their clinical relevance. Structural neuroplasticity is explored through changes in brain volume, cortical thickness, and white matter properties, presenting ECT as a potent stimulator of brain architecture alterations. Functional plasticity examines ECT's impact on brain function through diverse neuroimaging techniques, suggesting significant yet complex modifications in brain network connectivity and activity. The review emphasizes the multilevel nature of these neuroplasticity levels and their collective role in ECT's therapeutic outcomes. Methodological considerations—including sample size, patient heterogeneity, and variability in assessment timing—emerge as recurring themes in the literature, underscoring the need for more consistent and rigorous research designs. By outlining a cohesive framework of changes in neuroplasticity due to ECT, this review provides initial steps towards a deeper comprehension of ECT's mechanisms.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106143"},"PeriodicalIF":7.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834478","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 : 2025-04-09DOI: 10.1016/j.neubiorev.2025.106146
Resh S. Gupta , Wendy Heller , Todd S. Braver
Prior research has provided initial support for the claim that cognitive control mediates the relationship between anxiety and mindfulness; however, findings are often inconsistent. In this review, we argue that the inconsistency may be due to a lack of both conceptual and methodological precision in terms of how anxiety, cognitive control, and mindfulness are operationalized and assessed, and that this imprecision may be a critical source of study confounds and ambiguous outcomes. We unpack this argument by first decomposing anxiety, cognitive control, mindfulness, and relevant experimental paradigms into key dimensions in order to develop a non-unitary, multi-dimensional taxonomy of these constructs. Subsequently, we review and reinterpret the prior experimental literature, focusing on studies that examine the relationship between anxiety and cognitive control, mindfulness and cognitive control, and the three-way relationship between anxiety, mindfulness, and cognitive control. Across the reviewed studies, there was great variation in the dimensions being examined and the behavioral and/or neural measures employed; therefore, results were often mixed. Based on this review of literature, we propose a conceptually and methodologically precise framework from which to study the effects of mindfulness on cognitive control in anxiety. The framework theoretically aligns anxiety dimensions with specific mindfulness states and interventions, further suggesting how these will impact specific cognitive control dimensions (proactive, reactive). These can be assessed with experimental paradigms and associated behavioral and neural metrics to index the relevant dimensions with high precision. Novel experimental studies and tractable research designs are also proposed to rigorously test this theoretical framework.
{"title":"Reconceptualizing the relationship between anxiety, mindfulness, and cognitive control","authors":"Resh S. Gupta , Wendy Heller , Todd S. Braver","doi":"10.1016/j.neubiorev.2025.106146","DOIUrl":"10.1016/j.neubiorev.2025.106146","url":null,"abstract":"<div><div>Prior research has provided initial support for the claim that cognitive control mediates the relationship between anxiety and mindfulness; however, findings are often inconsistent. In this review, we argue that the inconsistency may be due to a lack of both conceptual and methodological precision in terms of how anxiety, cognitive control, and mindfulness are operationalized and assessed, and that this imprecision may be a critical source of study confounds and ambiguous outcomes. We unpack this argument by first decomposing anxiety, cognitive control, mindfulness, and relevant experimental paradigms into key dimensions in order to develop a non-unitary, multi-dimensional taxonomy of these constructs. Subsequently, we review and reinterpret the prior experimental literature, focusing on studies that examine the relationship between anxiety and cognitive control, mindfulness and cognitive control, and the three-way relationship between anxiety, mindfulness, and cognitive control. Across the reviewed studies, there was great variation in the dimensions being examined and the behavioral and/or neural measures employed; therefore, results were often mixed. Based on this review of literature, we propose a conceptually and methodologically precise framework from which to study the effects of mindfulness on cognitive control in anxiety. The framework theoretically aligns anxiety dimensions with specific mindfulness states and interventions, further suggesting how these will impact specific cognitive control dimensions (proactive, reactive). These can be assessed with experimental paradigms and associated behavioral and neural metrics to index the relevant dimensions with high precision. Novel experimental studies and tractable research designs are also proposed to rigorously test this theoretical framework.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106146"},"PeriodicalIF":7.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834480","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 : 2025-04-09DOI: 10.1016/j.neubiorev.2025.106142
Erica N. Grodin , Hollis Karoly , Brittney D. Browning , Leon Coleman , Mehdi Farokhnia , Lindsay A. Kryszak , Lindsay R. Meredith , Lindsay M. Squeglia
A large body of evidence suggests that heavy alcohol use is associated with dysregulated immune function, and that immune dysfunction in turn contributes to the pathophysiology of alcohol use disorder (AUD). As such, alcohol researchers have increasingly begun to include measurements of immune function—primarily peripheral circulating cytokines—in human studies, with the goal of testing associations with clinically-relevant behavioral measures. To date, findings and implications from these studies have been inconsistent and difficult to interpret, likely due to methodological challenges related to study design and implementation. In particular, the existing literature has demonstrated sample processing concerns, differences in assay methods, limited selection of analytes, and sample selection biases, all of which may contribute to inconsistent results. We briefly review the field, discuss these and other challenges, and propose guidance for designing studies on inflammation among heavy-drinking human participants. We note that conducting such studies requires appreciable consideration and planning, and ideally should involve an interdisciplinary team of experts, including immunologists, physiologists, and technical experts in bioassays, alongside experts in the field of interest (e.g., AUD). We highlight the importance of considering participant selection, analyte selection, sample collection, sample handling and storage, and assay methods, and suggest that the field move towards standardization of procedures and reporting. We propose that undertaking these changes in study design and implementation should produce consilience in findings and aid in our overall understanding of the complex relationship between alcohol exposure and immune function.
{"title":"Utilizing blood inflammatory markers in alcohol studies: Considerations and recommendations for study design, sample collection, and data analysis","authors":"Erica N. Grodin , Hollis Karoly , Brittney D. Browning , Leon Coleman , Mehdi Farokhnia , Lindsay A. Kryszak , Lindsay R. Meredith , Lindsay M. Squeglia","doi":"10.1016/j.neubiorev.2025.106142","DOIUrl":"10.1016/j.neubiorev.2025.106142","url":null,"abstract":"<div><div>A large body of evidence suggests that heavy alcohol use is associated with dysregulated immune function, and that immune dysfunction in turn contributes to the pathophysiology of alcohol use disorder (AUD). As such, alcohol researchers have increasingly begun to include measurements of immune function—primarily peripheral circulating cytokines—in human studies, with the goal of testing associations with clinically-relevant behavioral measures. To date, findings and implications from these studies have been inconsistent and difficult to interpret, likely due to methodological challenges related to study design and implementation. In particular, the existing literature has demonstrated sample processing concerns, differences in assay methods, limited selection of analytes, and sample selection biases, all of which may contribute to inconsistent results. We briefly review the field, discuss these and other challenges, and propose guidance for designing studies on inflammation among heavy-drinking human participants. We note that conducting such studies requires appreciable consideration and planning, and ideally should involve an interdisciplinary team of experts, including immunologists, physiologists, and technical experts in bioassays, alongside experts in the field of interest (e.g., AUD). We highlight the importance of considering participant selection, analyte selection, sample collection, sample handling and storage, and assay methods, and suggest that the field move towards standardization of procedures and reporting. We propose that undertaking these changes in study design and implementation should produce consilience in findings and aid in our overall understanding of the complex relationship between alcohol exposure and immune function.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106142"},"PeriodicalIF":7.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834482","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 : 2025-04-09DOI: 10.1016/j.neubiorev.2025.106141
Idil Sezer , Matthew D. Sacchet
Meditation has become prominent in both clinical and non-clinical applications for its effects on psychological and physical well-being. Long-term meditators, who have dedicated extensive time to their practice, present a unique opportunity to explore the effects of prolonged meditation training on the autonomic nervous system. Research has reported concomitant activation of both sympathetic (aroused) and parasympathetic (relaxed) branches of the autonomic nervous system during some forms of meditation, leading to the term ‘relaxed alertness.’ However, findings are not consistent, with reports of both sympathetic and parasympathetic activation, sympathetic-only, parasympathetic-only, or temporally variable activations, depending on several factors. This review synthesizes these heterogeneous and seemingly inconsistent results in relation to three explanatory factors: (1) specific classification of style or type of meditation; (2) specific definition of the level of expertise of the meditators; and (3) intra-individual variations within a given meditation practice. When these factors are considered, convergent and meaningful patterns emerge, allowing for a shift from the broad notion of 'long-term' meditation to a more precise characterization of 'advanced' meditation, highlighting skills, states, and stages of mastery developed over time. Our synthesis is particularly useful for understanding both long-term and advanced meditation, as it reveals specific heart rate variability patterns, including very low and low-frequency spectral power peaks, along with cardiac and respiratory coupling. Better characterization of the role of the autonomic nervous system in the context of advanced meditation promises to inform improved meditation training, including training assisted by technology, toward more impactful outcomes.
{"title":"Advanced and long-term meditation and the autonomic nervous system: A review and synthesis","authors":"Idil Sezer , Matthew D. Sacchet","doi":"10.1016/j.neubiorev.2025.106141","DOIUrl":"10.1016/j.neubiorev.2025.106141","url":null,"abstract":"<div><div>Meditation has become prominent in both clinical and non-clinical applications for its effects on psychological and physical well-being. Long-term meditators, who have dedicated extensive time to their practice, present a unique opportunity to explore the effects of prolonged meditation training on the autonomic nervous system. Research has reported concomitant activation of both sympathetic (aroused) and parasympathetic (relaxed) branches of the autonomic nervous system during some forms of meditation, leading to the term ‘relaxed alertness.’ However, findings are not consistent, with reports of both sympathetic and parasympathetic activation, sympathetic-only, parasympathetic-only, or temporally variable activations, depending on several factors. This review synthesizes these heterogeneous and seemingly inconsistent results in relation to three explanatory factors: (1) specific classification of style or type of meditation; (2) specific definition of the level of expertise of the meditators; and (3) intra-individual variations within a given meditation practice. When these factors are considered, convergent and meaningful patterns emerge, allowing for a shift from the broad notion of 'long-term' meditation to a more precise characterization of 'advanced' meditation, highlighting skills, states, and stages of mastery developed over time. Our synthesis is particularly useful for understanding both long-term and advanced meditation, as it reveals specific heart rate variability patterns, including very low and low-frequency spectral power peaks, along with cardiac and respiratory coupling. Better characterization of the role of the autonomic nervous system in the context of advanced meditation promises to inform improved meditation training, including training assisted by technology, toward more impactful outcomes.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106141"},"PeriodicalIF":7.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816002","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 : 2025-04-09DOI: 10.1016/j.neubiorev.2025.106138
Jayne Morriss
Intolerance of uncertainty (IU), the tendency to find uncertainty negative, is a fundamental transdiagnostic dimension across anxiety-related disorders. Over the past two decades, there has been an increase in both clinical and experimental research on the role of IU in the maintenance and treatment of anxiety-related disorders. However, there has been a lack of integration of research findings from a mechanistic perspective, which has slowed progress in translational research. This review seeks to fill this gap by synthesising the clinical (e.g. randomised controlled trials) and experimental (e.g. lab-based) literature on the psychological mechanisms that drive change in IU across anxiety-related disorders. The review highlighted that: (1) cognitive restructuring, supported by mechanisms such as cognitive appraisal, modify IU-related cognitions, (2) behavioural exposures, supported by mechanisms such as inhibitory learning, alter IU-related cognitions and physiological arousal, and (3) mindfulness techniques underpinned by mechanisms such as attentional monitoring, decentering, and acceptance, change IU-related cognitions. Across the different therapeutic techniques reviewed, there was a lack of evidence for how different mechanisms change IU-related emotions and behaviours. Directions for further research include directly comparing the effectiveness of different mechanisms that produce change in IU across anxiety disorders and other mental health disorders, and examining the specificity of change in IU over other anxious traits. Overall, the findings provide a foundation for future translational research efforts to build upon maximising existing treatment interventions and/or to develop novel treatment interventions to target dispositional IU and situational uncertainty-related distress in anxiety-related disorders and beyond.
对不确定性的不容忍（IU），即认为不确定性是负面的倾向，是焦虑相关障碍的一个基本跨诊断维度。过去二十年来，关于不确定性不容忍在焦虑相关障碍的维持和治疗中的作用的临床和实验研究不断增加。然而，由于缺乏从机理角度对研究结果进行整合，导致转化研究进展缓慢。本综述试图通过综合临床（如随机对照试验）和实验（如基于实验室的）文献来填补这一空白，这些文献涉及了推动焦虑相关障碍中IU变化的心理机制。综述强调(1) 在认知评估等机制的支持下，认知重组改变了与 IU 相关的认知；(2) 在抑制性学习等机制的支持下，行为暴露改变了与 IU 相关的认知和生理唤醒；(3) 在注意力监测、去中心化和接受等机制的支持下，正念技术改变了与 IU 相关的认知。在所审查的不同治疗技术中，缺乏关于不同机制如何改变与 IU 相关的情绪和行为的证据。进一步研究的方向包括：直接比较不同机制对焦虑症和其他心理健康疾病产生 IU 变化的有效性，以及研究 IU 变化相对于其他焦虑特征的特异性。总之，这些研究结果为未来的转化研究工作奠定了基础，以便在最大限度地利用现有治疗干预措施的基础上，和/或开发新型治疗干预措施，针对焦虑相关疾病及其他疾病中的倾向性IU和情境不确定性相关困扰进行治疗。
{"title":"Psychological mechanisms underpinning change in intolerance of uncertainty across anxiety-related disorders: New insights for translational research","authors":"Jayne Morriss","doi":"10.1016/j.neubiorev.2025.106138","DOIUrl":"10.1016/j.neubiorev.2025.106138","url":null,"abstract":"<div><div>Intolerance of uncertainty (IU), the tendency to find uncertainty negative, is a fundamental transdiagnostic dimension across anxiety-related disorders. Over the past two decades, there has been an increase in both clinical and experimental research on the role of IU in the maintenance and treatment of anxiety-related disorders. However, there has been a lack of integration of research findings from a mechanistic perspective, which has slowed progress in translational research. This review seeks to fill this gap by synthesising the clinical (e.g. randomised controlled trials) and experimental (e.g. lab-based) literature on the psychological mechanisms that drive change in IU across anxiety-related disorders. The review highlighted that: (1) cognitive restructuring, supported by mechanisms such as cognitive appraisal, modify IU-related cognitions, (2) behavioural exposures, supported by mechanisms such as inhibitory learning, alter IU-related cognitions and physiological arousal, and (3) mindfulness techniques underpinned by mechanisms such as attentional monitoring, decentering, and acceptance, change IU-related cognitions. Across the different therapeutic techniques reviewed, there was a lack of evidence for how different mechanisms change IU-related emotions and behaviours. Directions for further research include directly comparing the effectiveness of different mechanisms that produce change in IU across anxiety disorders and other mental health disorders, and examining the specificity of change in IU over other anxious traits. Overall, the findings provide a foundation for future translational research efforts to build upon maximising existing treatment interventions and/or to develop novel treatment interventions to target dispositional IU and situational uncertainty-related distress in anxiety-related disorders and beyond.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106138"},"PeriodicalIF":7.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821130","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 : 2025-04-07DOI: 10.1016/j.neubiorev.2025.106139
Georg Northoff , Bianca Ventura
Neuroscience faces the challenge of connecting brain and mind, with the mind manifesting in first-person experience while the brain’s neural activity can only be investigated in third-person perspective. To connect neural and mental states, Neurophenomenology provides a methodological toolkit for systematically linking first-person subjective experience with third-person objective observations of the brain’s neural activity. However, beyond providing a systematic methodological strategy (‘disciplined circularity’), it leaves open how neural activity and subjective experience are related among themselves, independent of our methodological strategy. The recently introduced Spatiotemporal Neuroscience suggests that neural activity and subjective experience share a commonly underlying feature as their “common currency”, notably analogous spatiotemporal dynamics. Can Spatiotemporal Neuroscience inform Neurophenomenology to allow for a deeper and more substantiative connection of first-person experience and third-person neural activity? The goal of our paper is to show how Spatiotemporal Neuroscience and Neurophenomenology can be converged and integrated with each other to gain better understanding of the brain-mind connection. We describe their convergence on theoretical grounds which, subsequently, is illustrated by empirical examples like self, meditation, and depression. In conclusion, we propose that the integration of Neurophenomenology and Spatiotemporal Neuroscience can provide complementary insights, enrich both fields, allows for deeper understanding of brain-mind connection, and opens the door for developing novel methodological approaches in their empirical investigation.
{"title":"Bridging the gap of brain and experience – Converging Neurophenomenology with Spatiotemporal Neuroscience","authors":"Georg Northoff , Bianca Ventura","doi":"10.1016/j.neubiorev.2025.106139","DOIUrl":"10.1016/j.neubiorev.2025.106139","url":null,"abstract":"<div><div>Neuroscience faces the challenge of connecting brain and mind, with the mind manifesting in first-person experience while the brain’s neural activity can only be investigated in third-person perspective. To connect neural and mental states, Neurophenomenology provides a methodological toolkit for systematically linking first-person subjective experience with third-person objective observations of the brain’s neural activity. However, beyond providing a systematic methodological strategy (‘disciplined circularity’), it leaves open how neural activity and subjective experience are related among themselves, independent of our methodological strategy. The recently introduced Spatiotemporal Neuroscience suggests that neural activity and subjective experience share a commonly underlying feature as their “common currency”, notably analogous spatiotemporal dynamics. Can Spatiotemporal Neuroscience inform Neurophenomenology to allow for a deeper and more substantiative connection of first-person experience and third-person neural activity? The goal of our paper is to show how Spatiotemporal Neuroscience and Neurophenomenology can be converged and integrated with each other to gain better understanding of the brain-mind connection. We describe their convergence on theoretical grounds which, subsequently, is illustrated by empirical examples like self, meditation, and depression. In conclusion, we propose that the integration of Neurophenomenology and Spatiotemporal Neuroscience can provide complementary insights, enrich both fields, allows for deeper understanding of brain-mind connection, and opens the door for developing novel methodological approaches in their empirical investigation.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106139"},"PeriodicalIF":7.5,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828896","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 : 2025-04-05DOI: 10.1016/j.neubiorev.2025.106131
Weiye Chen, Ian N. Johnston
People diagnosed with cancer who undergo chemotherapy commonly encounter cognitive changes, particularly in executive functions (EFs). EFs support goal-directed behaviours, with EF deficits implicated in various neurocognitive impairments. We conducted five meta-analyses of the rodent models to investigate the impact of chemotherapy across five EF domains. A systematic search across PubMed, Web of Science, Scopus, and PsycINFO yielded 56 eligible papers. Our findings supported the clinical literature suggesting the selective impact of chemotherapy on different EF domains. Specifically, chemotherapy-treated animals performed significantly more poorly than controls in tasks assessing working memory, behavioural flexibility, and problem-solving, with no significant group differences in inhibition or attention. Subgroup analyses revealed that alkylating agents, antitumor antibiotics, and combination therapies were strongly associated with working memory deficits, whereas mitotic inhibitors were not. Rodent species, strain, age, sex, number of treatments, and time of behavioural assessment since the end of treatment did not moderate the drug effect on any assessed EF domains. To increase the generalisability and translational validity of the results, the overall reporting quality of animal studies needs to be improved with more details on randomisation, blinding, sample sizes, and criteria for animal exclusions.
{"title":"Meta-analyses of executive function deficits in chemotherapy-treated rodent models","authors":"Weiye Chen, Ian N. Johnston","doi":"10.1016/j.neubiorev.2025.106131","DOIUrl":"10.1016/j.neubiorev.2025.106131","url":null,"abstract":"<div><div>People diagnosed with cancer who undergo chemotherapy commonly encounter cognitive changes, particularly in executive functions (EFs). EFs support goal-directed behaviours, with EF deficits implicated in various neurocognitive impairments. We conducted five meta-analyses of the rodent models to investigate the impact of chemotherapy across five EF domains. A systematic search across PubMed, Web of Science, Scopus, and PsycINFO yielded 56 eligible papers. Our findings supported the clinical literature suggesting the selective impact of chemotherapy on different EF domains. Specifically, chemotherapy-treated animals performed significantly more poorly than controls in tasks assessing working memory, behavioural flexibility, and problem-solving, with no significant group differences in inhibition or attention. Subgroup analyses revealed that alkylating agents, antitumor antibiotics, and combination therapies were strongly associated with working memory deficits, whereas mitotic inhibitors were not. Rodent species, strain, age, sex, number of treatments, and time of behavioural assessment since the end of treatment did not moderate the drug effect on any assessed EF domains. To increase the generalisability and translational validity of the results, the overall reporting quality of animal studies needs to be improved with more details on randomisation, blinding, sample sizes, and criteria for animal exclusions.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"173 ","pages":"Article 106131"},"PeriodicalIF":7.5,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804935","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 : 2025-04-04DOI: 10.1016/j.neubiorev.2025.106123
F.M. Kausche, H.P. Carsten, K.M. Sobania, A. Riesel
{"title":"Corrigendum to “Fear and safety learning in anxiety- and stress-related disorders: An updated meta-analysis” [Neurosci. Biobehav. Rev. 169 (2025) 105983]","authors":"F.M. Kausche, H.P. Carsten, K.M. Sobania, A. Riesel","doi":"10.1016/j.neubiorev.2025.106123","DOIUrl":"10.1016/j.neubiorev.2025.106123","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"172 ","pages":"Article 106123"},"PeriodicalIF":7.5,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789385","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 : 2025-04-03DOI: 10.1016/j.neubiorev.2025.106137
Sophie Nolden, Oded Bein, Yee Lee Shing
{"title":"Priors, Evidence, and Memory: Dynamics of Predictive Processing (POEM).","authors":"Sophie Nolden, Oded Bein, Yee Lee Shing","doi":"10.1016/j.neubiorev.2025.106137","DOIUrl":"https://doi.org/10.1016/j.neubiorev.2025.106137","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":" ","pages":"106137"},"PeriodicalIF":7.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789387","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}
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