Pub Date : 2025-02-01DOI: 10.1016/j.neubiorev.2024.105996
Marie-Christin Barthel , Kim Fricke , Markus Muehlhan , Susanne Vogel , Nina Alexander
Recurrent psychosocial stress poses a significant health challenge, prompting research into mechanisms of successful adaptation. Physiological habituation, defined as decreased reactivity to repeated stressors, is pivotal in protecting the organism from allostatic load. Here, we systematically review and meta-analyze data from studies investigating the capacity of central stress systems to habituate when repeatedly exposed to a standardized psychosocial stressor, the Trier Social Stress Test (k = 47). For a comprehensive overview of biological stress systems, we examine multiple markers of the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system (ANS), and the immune system. Our findings indicate that habituation patterns vary substantially between different stress systems. While most studies provide robust evidence for rapid and substantial HPA-axis habituation, ANS and immune marker responses to repeated stress are less uniform. We further integrate existing knowledge on personal and environmental influences contributing to individual differences in habituation capacity. Additionally, we discuss the implications of stress habituation patterns for health outcomes and the design of longitudinal stress studies and highlight potential avenues for future research.
{"title":"Habituation of the biological response to repeated psychosocial stress: a systematic review and meta-analysis","authors":"Marie-Christin Barthel , Kim Fricke , Markus Muehlhan , Susanne Vogel , Nina Alexander","doi":"10.1016/j.neubiorev.2024.105996","DOIUrl":"10.1016/j.neubiorev.2024.105996","url":null,"abstract":"<div><div>Recurrent psychosocial stress poses a significant health challenge, prompting research into mechanisms of successful adaptation. Physiological habituation, defined as decreased reactivity to repeated stressors, is pivotal in protecting the organism from allostatic load. Here, we systematically review and meta-analyze data from studies investigating the capacity of central stress systems to habituate when repeatedly exposed to a standardized psychosocial stressor, the Trier Social Stress Test (k = 47). For a comprehensive overview of biological stress systems, we examine multiple markers of the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system (ANS), and the immune system. Our findings indicate that habituation patterns vary substantially between different stress systems. While most studies provide robust evidence for rapid and substantial HPA-axis habituation, ANS and immune marker responses to repeated stress are less uniform. We further integrate existing knowledge on personal and environmental influences contributing to individual differences in habituation capacity. Additionally, we discuss the implications of stress habituation patterns for health outcomes and the design of longitudinal stress studies and highlight potential avenues for future research.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105996"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928810","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.2025.106003
Abigail O. Vogeley , Alicia A. Livinski , Shahaboddin Dabaghi Varnosfaderani , Nooshin Javaheripour , Hamidreza Jamalabadi , Vasileia Kotoula , Ioline D. Henter , Nadia S. Hejazi , Rebecca B. Price , Mani Yavi , Martin Walter , Carlos A. Zarate Jr , Mina Kheirkhah
Understanding how the brain distinguishes emotional from neutral scenes is crucial for advancing brain-computer interfaces, enabling real-time emotion detection for faster, more effective responses, and improving treatments for emotional disorders like depression and anxiety. However, inconsistent research findings have arisen from differences in study settings, such as variations in the time windows, brain regions, and emotion categories examined across studies. This review sought to compile the existing literature on the timing at which the adult brain differentiates basic affective from neutral scenes in less than one second, as previous studies have consistently shown that the brain can begin recognizing emotions within just a few milliseconds. The review includes studies that used electroencephalography (EEG) or magnetoencephalography (MEG) in healthy adults to examine brain responses to emotional versus neutral images within one second. Articles of interest were limited to the English language but not to any publication year. Excluded studies involved only patients (of any diagnosis), participants under age 18 (since emotional processing can differ between adults and younger individuals), non-passive tasks, low temporal resolution techniques, time intervals over one second, and animals. Of the 3045 screened articles, 19 met these criteria. Despite the variations between studies, the earliest onset for heightened brain responses to basic affective scenes compared to neutral ones was most commonly observed within the 250–300 ms time window. To the best of our knowledge, this review is the first to synthesize data on the timing of brain differentiation between emotional and neutral scenes in healthy adults.
{"title":"Temporal dynamics of affective scene processing in the healthy adult human brain","authors":"Abigail O. Vogeley , Alicia A. Livinski , Shahaboddin Dabaghi Varnosfaderani , Nooshin Javaheripour , Hamidreza Jamalabadi , Vasileia Kotoula , Ioline D. Henter , Nadia S. Hejazi , Rebecca B. Price , Mani Yavi , Martin Walter , Carlos A. Zarate Jr , Mina Kheirkhah","doi":"10.1016/j.neubiorev.2025.106003","DOIUrl":"10.1016/j.neubiorev.2025.106003","url":null,"abstract":"<div><div>Understanding how the brain distinguishes emotional from neutral scenes is crucial for advancing brain-computer interfaces, enabling real-time emotion detection for faster, more effective responses, and improving treatments for emotional disorders like depression and anxiety. However, inconsistent research findings have arisen from differences in study settings, such as variations in the time windows, brain regions, and emotion categories examined across studies. This review sought to compile the existing literature on the timing at which the adult brain differentiates basic affective from neutral scenes in less than one second, as previous studies have consistently shown that the brain can begin recognizing emotions within just a few milliseconds. The review includes studies that used electroencephalography (EEG) or magnetoencephalography (MEG) in healthy adults to examine brain responses to emotional versus neutral images within one second. Articles of interest were limited to the English language but not to any publication year. Excluded studies involved only patients (of any diagnosis), participants under age 18 (since emotional processing can differ between adults and younger individuals), non-passive tasks, low temporal resolution techniques, time intervals over one second, and animals. Of the 3045 screened articles, 19 met these criteria. Despite the variations between studies, the earliest onset for heightened brain responses to basic affective scenes compared to neutral ones was most commonly observed within the 250–300 ms time window. To the best of our knowledge, this review is the first to synthesize data on the timing of brain differentiation between emotional and neutral scenes in healthy adults.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106003"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928816","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.2025.106019
Sawsan Aboul-Fotouh , Sohir M. Zohny , Esraa M. Elnahas , Mohamed Z. Habib , Ghada AM. Hassan
Autism Spectrum Disorder (ASD) represents a clinical challenge due to its diverse behavioral symptoms and complex neuro-pathophysiology. Finding effective treatments that target the fundamental mechanisms of ASD remains a top priority. This narrative review presents the potential of the NMDA-receptor blocker memantine in managing ASD symptoms. Preclinical studies indicate that memantine could abrogate excitotoxicity, GABA/glutamate imbalance, reduced levels of brain-derived neurotrophic factor (BDNF), blood-brain barrier (BBB) leakage, and neuroinflammation, offering hope for managing core deficits associated with ASD like impaired social interaction and repetitive behaviors. However, clinical trials yield conflicting results, with some showing slight improvements in symptom severity and cognitive function, while others demonstrate limited efficacy. Further exploration of memantine's neurobiological mechanisms and refinement of treatment approaches are crucial for comprehensively tackling ASD complexities. Drawing from both animal models and clinical data, this review examines memantine's impact on core ASD symptoms, cognitive function, and potential mechanisms of action. Lastly, it identifies research gaps and proposes avenues for future investigations to enhance our understanding and utilization of memantine in ASD management.
{"title":"Can memantine treat autism? Answers from preclinical and clinical studies","authors":"Sawsan Aboul-Fotouh , Sohir M. Zohny , Esraa M. Elnahas , Mohamed Z. Habib , Ghada AM. Hassan","doi":"10.1016/j.neubiorev.2025.106019","DOIUrl":"10.1016/j.neubiorev.2025.106019","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) represents a clinical challenge due to its diverse behavioral symptoms and complex neuro-pathophysiology. Finding effective treatments that target the fundamental mechanisms of ASD remains a top priority. This narrative review presents the potential of the NMDA-receptor blocker memantine in managing ASD symptoms. Preclinical studies indicate that memantine could abrogate excitotoxicity, GABA/glutamate imbalance, reduced levels of brain-derived neurotrophic factor (BDNF), blood-brain barrier (BBB) leakage, and neuroinflammation, offering hope for managing core deficits associated with ASD like impaired social interaction and repetitive behaviors. However, clinical trials yield conflicting results, with some showing slight improvements in symptom severity and cognitive function, while others demonstrate limited efficacy. Further exploration of memantine's neurobiological mechanisms and refinement of treatment approaches are crucial for comprehensively tackling ASD complexities. Drawing from both animal models and clinical data, this review examines memantine's impact on core ASD symptoms, cognitive function, and potential mechanisms of action. Lastly, it identifies research gaps and proposes avenues for future investigations to enhance our understanding and utilization of memantine in ASD management.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106019"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017056","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}
Substance abuse research depends on precise and sensitive assessments of reinforcer efficacy in animal models. However, conventional methods often lack theoretical rigor and specificity to support these assessments. To address these gaps, the Modular Maximization Theory (MMT) is introduced as a comprehensive framework for understanding instrumental behavior. Like earlier maximization theories, MMT posits that behavior is distributed across alternatives to maximize utility over time. This concept is structured through five foundational postulates that define alternative actions and rules for choosing between them as budget constraints and utility functions. A key innovation of MMT is its incorporation of reinforcer utilization—encompassing both consummatory and post-consummatory activities—into the budget-constraint function. A model of ratio-schedule performance is developed under the assumption that utilization is proportional to demand, with utility represented as an additive power function of reinforcer magnitude. This model, termed PURSPU (Proportional Utilization, Ratio Schedule, Power Utility), effectively explains how reinforcer magnitude, response effort, non-contingent reinforcement, and income influence demand curves, behavior-output functions, dose-response relationships, and progressive-ratio breakpoints, while accounting for rate-dependent effects. The model also offers novel insights into choice behavior, including concurrent-schedule performance, income dependency, and delay discounting, as well as post-reinforcement pauses and run rates. Variations in budget constraints and utility functions are proposed as alternative models. Potential theoretical advancements, more targeted assessments of drug abuse liability, and the broader role of MMT in understanding human drug abuse are explored.
{"title":"Modular Maximization Theory: A functional account of economic behavior in laboratory animal models with applications to drug-seeking behavior","authors":"Federico Sanabria , Matthew Gildea , Brissa Gutiérrez , Cristina Santos , Adeline Hibshman","doi":"10.1016/j.neubiorev.2025.106010","DOIUrl":"10.1016/j.neubiorev.2025.106010","url":null,"abstract":"<div><div>Substance abuse research depends on precise and sensitive assessments of reinforcer efficacy in animal models. However, conventional methods often lack theoretical rigor and specificity to support these assessments. To address these gaps, the Modular Maximization Theory (MMT) is introduced as a comprehensive framework for understanding instrumental behavior. Like earlier maximization theories, MMT posits that behavior is distributed across alternatives to maximize utility over time. This concept is structured through five foundational postulates that define alternative actions and rules for choosing between them as budget constraints and utility functions. A key innovation of MMT is its incorporation of reinforcer utilization—encompassing both consummatory and post-consummatory activities—into the budget-constraint function. A model of ratio-schedule performance is developed under the assumption that utilization is proportional to demand, with utility represented as an additive power function of reinforcer magnitude. This model, termed PURSPU (Proportional Utilization, Ratio Schedule, Power Utility), effectively explains how reinforcer magnitude, response effort, non-contingent reinforcement, and income influence demand curves, behavior-output functions, dose-response relationships, and progressive-ratio breakpoints, while accounting for rate-dependent effects. The model also offers novel insights into choice behavior, including concurrent-schedule performance, income dependency, and delay discounting, as well as post-reinforcement pauses and run rates. Variations in budget constraints and utility functions are proposed as alternative models. Potential theoretical advancements, more targeted assessments of drug abuse liability, and the broader role of MMT in understanding human drug abuse are explored.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106010"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017085","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.2025.106011
Sofia Tzioridou , Teresa Campillo-Ferrer , Jorge Cañas-Martín , Linda Schlüter , Susana G. Torres-Platas , Jarrod A. Gott , Nirit Soffer-Dudek , Tadas Stumbrys , Martin Dresler
During most dreams, the dreamer does not realize that they are in a dream. In contrast, lucid dreaming allows to become aware of the current state of mind, often accompanied by considerable control over the ongoing dream episode. Lucid dreams can happen spontaneously or be induced through diverse behavioural, cognitive or technological strategies. Such induction techniques have spurred research into the potential therapeutic aspects of lucid dreams. In this review, we gather evidence on the link between lucid dreams and conditions like nightmare disorder, depression, anxiety, psychosis, and dissociative states, and highlight the possible neurobiological basis of these associations. Furthermore, we explore contemplative sleep practices that train lucid states during sleep, such as Dream/Sleep Yoga and Yoga Nidrâ. The potential drawbacks of lucid dreaming interventions are outlined, accompanied by an examination of the impacts of lucid dreams on individuals without clinical conditions. By shedding light on these intricate relationships, the review contributes to a deeper understanding of the therapeutic possibilities and implications of lucid dreaming.
{"title":"The clinical neuroscience of lucid dreaming","authors":"Sofia Tzioridou , Teresa Campillo-Ferrer , Jorge Cañas-Martín , Linda Schlüter , Susana G. Torres-Platas , Jarrod A. Gott , Nirit Soffer-Dudek , Tadas Stumbrys , Martin Dresler","doi":"10.1016/j.neubiorev.2025.106011","DOIUrl":"10.1016/j.neubiorev.2025.106011","url":null,"abstract":"<div><div>During most dreams, the dreamer does not realize that they are in a dream. In contrast, lucid dreaming allows to become aware of the current state of mind, often accompanied by considerable control over the ongoing dream episode. Lucid dreams can happen spontaneously or be induced through diverse behavioural, cognitive or technological strategies. Such induction techniques have spurred research into the potential therapeutic aspects of lucid dreams. In this review, we gather evidence on the link between lucid dreams and conditions like nightmare disorder, depression, anxiety, psychosis, and dissociative states, and highlight the possible neurobiological basis of these associations. Furthermore, we explore contemplative sleep practices that train lucid states during sleep, such as Dream/Sleep Yoga and Yoga Nidrâ. The potential drawbacks of lucid dreaming interventions are outlined, accompanied by an examination of the impacts of lucid dreams on individuals without clinical conditions. By shedding light on these intricate relationships, the review contributes to a deeper understanding of the therapeutic possibilities and implications of lucid dreaming.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106011"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017115","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.2024.105997
Clara Salciccia , Matteo Costanzo , Giulia Ruocco , Flavia Porreca , Giorgio Vivacqua , Giovanni Fabbrini , Daniele Belvisi , Anna Ladogana , Anna Poleggi
A hallmark event in neurodegenerative diseases is represented by the misfolding, aggregation and accumulation of proteins, leading to cellular and network dysfunction preceding the development of clinical symptoms by years. Early diagnosis represents a crucial issue in the field of neuroscience as it offers the potential to utilize this therapeutic window in the future to manage disease-modifying therapy. Seed amplification assays, including Real-Time Quaking-Induced Conversion (RT-QuIC) and Protein Misfolding Cyclic Amplification (PMCA), have emerged in recent years as innovative techniques developed to detect minute amounts of amyloidogenic proteins. These techniques can utilize various biological fluids and tissues, with most evidence to date regarding their potential diagnostic use focusing on cerebrospinal fluid. In this scoping review, we aimed to investigate and discuss the available evidence regarding the diagnostic use of these assays on easily accessible biological fluids and tissues in patients affected by synucleinopathies, tauopathies or prion diseases. From a systematic search on two databases, Scopus and Pubmed, we identified 49 studies. Although most identified studies have used skin and olfactory mucosa as biological samples, there is preliminary evidence suggesting the potential implementation of these techniques using fluids as blood, saliva and tears. The results achieved so far, as well as methodological aspects and limitations to overcome, are discussed.
{"title":"Proteopathic seed amplification assays in easily accessible specimens for human synucleinopathies, tauopathies, and prionopathies: A scoping review","authors":"Clara Salciccia , Matteo Costanzo , Giulia Ruocco , Flavia Porreca , Giorgio Vivacqua , Giovanni Fabbrini , Daniele Belvisi , Anna Ladogana , Anna Poleggi","doi":"10.1016/j.neubiorev.2024.105997","DOIUrl":"10.1016/j.neubiorev.2024.105997","url":null,"abstract":"<div><div>A hallmark event in neurodegenerative diseases is represented by the misfolding, aggregation and accumulation of proteins, leading to cellular and network dysfunction preceding the development of clinical symptoms by years. Early diagnosis represents a crucial issue in the field of neuroscience as it offers the potential to utilize this therapeutic window in the future to manage disease-modifying therapy. Seed amplification assays, including Real-Time Quaking-Induced Conversion (RT-QuIC) and Protein Misfolding Cyclic Amplification (PMCA), have emerged in recent years as innovative techniques developed to detect minute amounts of amyloidogenic proteins. These techniques can utilize various biological fluids and tissues, with most evidence to date regarding their potential diagnostic use focusing on cerebrospinal fluid. In this scoping review, we aimed to investigate and discuss the available evidence regarding the diagnostic use of these assays on easily accessible biological fluids and tissues in patients affected by synucleinopathies, tauopathies or prion diseases. From a systematic search on two databases, Scopus and Pubmed, we identified 49 studies. Although most identified studies have used skin and olfactory mucosa as biological samples, there is preliminary evidence suggesting the potential implementation of these techniques using fluids as blood, saliva and tears. The results achieved so far, as well as methodological aspects and limitations to overcome, are discussed.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105997"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142924157","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.2025.106038
Sophia J. Weber , Marco Venniro
{"title":"It takes two: The interplay between dopamine and oxytocin in social behavior","authors":"Sophia J. Weber , Marco Venniro","doi":"10.1016/j.neubiorev.2025.106038","DOIUrl":"10.1016/j.neubiorev.2025.106038","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"170 ","pages":"Article 106038"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124230","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.2025.106001
Christian Keysers , Valeria Gazzola
{"title":"Neurobiology of social interactions across species","authors":"Christian Keysers , Valeria Gazzola","doi":"10.1016/j.neubiorev.2025.106001","DOIUrl":"10.1016/j.neubiorev.2025.106001","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 106001"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959249","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.2023.105331
Lavinia Teixeira-Machado , Ricardo Mario Arida , Jair de Jesus Mari
{"title":"Corrigendum to: “Dance for neuroplasticity: A descriptive systematic review” [Neurosci. Biobehav. Rev. 2019 Jan;96:232–240]","authors":"Lavinia Teixeira-Machado , Ricardo Mario Arida , Jair de Jesus Mari","doi":"10.1016/j.neubiorev.2023.105331","DOIUrl":"10.1016/j.neubiorev.2023.105331","url":null,"abstract":"","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105331"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793130","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.2024.105984
Thomas Parr , Ashwini Oswal , Sanjay G. Manohar
Most of our movement consists of sequences of discrete actions at regular intervals—including speech, walking, playing music, or even chewing. Despite this, few models of the motor system address how the brain determines the interval at which to trigger actions. This paper offers a theoretical analysis of the problem of timing movements. We consider a scenario in which we must align an alternating movement with a regular external (auditory) stimulus. We assume that our brains employ generative world models that include internal clocks of various speeds. These allow us to associate a temporally regular sensory input with an internal clock, and actions with parts of that clock cycle. We treat this as process of inferring which clock best explains sensory input. This offers a way in which temporally discrete choices might emerge from a continuous process. This is not straightforward, particularly if each of those choices unfolds during a time that has a (possibly unknown) duration. We develop a route for translation to neurology, in the context of Parkinson’s disease—a disorder that characteristically slows down movements. The effects are often elicited in clinic by alternating movements. We find that it is possible to reproduce behavioural and electrophysiological features associated with parkinsonism by disrupting specific parameters—that determine the priors for inferences made by the brain. We observe three core features of Parkinson’s disease: amplitude decrement, festination, and breakdown of repetitive movements. Our simulations provide a mechanistic interpretation of how pathology and therapeutics might influence behaviour and neural activity.
{"title":"Inferring when to move","authors":"Thomas Parr , Ashwini Oswal , Sanjay G. Manohar","doi":"10.1016/j.neubiorev.2024.105984","DOIUrl":"10.1016/j.neubiorev.2024.105984","url":null,"abstract":"<div><div>Most of our movement consists of sequences of discrete actions at regular intervals—including speech, walking, playing music, or even chewing. Despite this, few models of the motor system address how the brain determines the interval at which to trigger actions. This paper offers a theoretical analysis of the problem of timing movements. We consider a scenario in which we must align an alternating movement with a regular external (auditory) stimulus. We assume that our brains employ generative world models that include internal clocks of various speeds. These allow us to associate a temporally regular sensory input with an internal clock, and actions with parts of that clock cycle. We treat this as process of inferring which clock best explains sensory input. This offers a way in which temporally discrete choices might emerge from a continuous process. This is not straightforward, particularly if each of those choices unfolds during a time that has a (possibly unknown) duration. We develop a route for translation to neurology, in the context of Parkinson’s disease—a disorder that characteristically slows down movements. The effects are often elicited in clinic by alternating movements. We find that it is possible to reproduce behavioural and electrophysiological features associated with parkinsonism by disrupting specific parameters—that determine the priors for inferences made by the brain. We observe three core features of Parkinson’s disease: amplitude decrement, festination, and breakdown of repetitive movements. Our simulations provide a mechanistic interpretation of how pathology and therapeutics might influence behaviour and neural activity.</div></div>","PeriodicalId":56105,"journal":{"name":"Neuroscience and Biobehavioral Reviews","volume":"169 ","pages":"Article 105984"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856965","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}
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