Stress is a ubiquitous facet of life. Ranging in form (e.g., psychosocial, physical, nutritional, economic) and longevity (e.g., acute, chronic), stressors affect the biology of those directly in their line of attack. As is becoming increasingly appreciated, the pernicious effects of stress echo across generations (Dias et al. 2015; Yehuda and Lehrner 2018; Jawaid et al. 2021; Dion et al. 2022; Zhou and Ryan 2023; Dias 2024). With a focus on learning and memory, this chapter addresses how stressors derail learning and memory in the generation directly exposed to them andin future generations. To do so, with a specific emphasis on associative fear conditioning in humans and rodents, we touch upon the relevance of extinction training in the aftermath of such conditioning and the recall of such extinction training as windows into normative and disrupted learning. Next, we briefly discuss underlying neuroanatomical substrates mediating these processes. We then draw attention to influences of postnatal, in utero, and pre-conceptional stress on learning and memory across generations. Finally, we briefly outline biological factors that underlie how learning and memory is derailed by these stressors.
压力是生活中无处不在的一面。压力源在形式(如心理社会、生理、营养、经济)和寿命(如急性、慢性)上影响直接处于其攻击线上的人的生物学。正如人们越来越认识到的那样,压力的有害影响会在几代人之间产生回响(Dias et al. 2015;Yehuda and Lehrner 2018;Jawaid等人2021;Dion et al. 2022;周和瑞恩2023;迪亚斯2024)。本章将重点放在学习和记忆上,讨论压力源是如何在直接接触它们的一代人和后代中破坏学习和记忆的。为了做到这一点,我们特别强调了人类和啮齿动物的联想恐惧条件反射,我们触及了在这种条件反射的后果中灭绝训练的相关性,以及这种灭绝训练的回忆作为规范和中断学习的窗口。接下来,我们简要讨论潜在的神经解剖学基质介导这些过程。然后,我们提请注意出生后,子宫内和孕前压力对学习和记忆的影响跨代。最后,我们简要概述了这些压力源如何影响学习和记忆的生物学因素。
{"title":"Intergenerational Effects of Stress - A Focus on Learning and Memory.","authors":"L S Vasquez, S Stack, W W Taylor, B G Dias","doi":"10.1007/7854_2025_578","DOIUrl":"10.1007/7854_2025_578","url":null,"abstract":"<p><p>Stress is a ubiquitous facet of life. Ranging in form (e.g., psychosocial, physical, nutritional, economic) and longevity (e.g., acute, chronic), stressors affect the biology of those directly in their line of attack. As is becoming increasingly appreciated, the pernicious effects of stress echo across generations (Dias et al. 2015; Yehuda and Lehrner 2018; Jawaid et al. 2021; Dion et al. 2022; Zhou and Ryan 2023; Dias 2024). With a focus on learning and memory, this chapter addresses how stressors derail learning and memory in the generation directly exposed to them andin future generations. To do so, with a specific emphasis on associative fear conditioning in humans and rodents, we touch upon the relevance of extinction training in the aftermath of such conditioning and the recall of such extinction training as windows into normative and disrupted learning. Next, we briefly discuss underlying neuroanatomical substrates mediating these processes. We then draw attention to influences of postnatal, in utero, and pre-conceptional stress on learning and memory across generations. Finally, we briefly outline biological factors that underlie how learning and memory is derailed by these stressors.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"231-251"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The topic of my chapter will be Bud Craig's theory of "global emotional moments" (henceforth the GEMs theory) and the relationship of GEMs to the experience of time. I connect three ideas prominent in Craig's writings: interoception, emotion, and time. Craig held that each GEM has as its neural substrate a large-scale network with the anterior insula cortex (AIC) serving as its central processing hub. This network integrates interoceptive signals that keep track of changes arising in the autonomic nervous system with hedonic and motivational signals based on the organism's sensory perception of its environment. Craig argued that GEMs function as moving windows of time within which "a phenomenal self" is experienced. By the "phenomenal self," I mean a material, embodied self that forms an organism's subjective point of view on the world. Craig proposed what he called a "cinemascopic" theory of GEMs. GEMs are combined over time to form a stream of consciousness, which Craig compared to a movie, with each GEM corresponding to a single snapshot of this movie. I will argue that Craig's cinemascopic theory has implications for our understanding of what I will call the "phenomenal now." There are three main theories of the phenomenal now in the philosophical literature. One point of contention between these theories is whether the phenomenal now has duration or temporal depth. I will argue that GEMs have duration and therefore count against so-called "cinematic" theories of the phenomenal now that take the contents of experience to be of discrete points or instances in time. However, there are different views within philosophy of how the phenomenal now can have duration. I end my chapter by considering how Craig's GEMs theory might bear on this debate.
{"title":"Body, Self, and Time: Bud Craig's Global Emotional Moments Theory.","authors":"Julian Kiverstein","doi":"10.1007/7854_2024_575","DOIUrl":"10.1007/7854_2024_575","url":null,"abstract":"<p><p>The topic of my chapter will be Bud Craig's theory of \"global emotional moments\" (henceforth the GEMs theory) and the relationship of GEMs to the experience of time. I connect three ideas prominent in Craig's writings: interoception, emotion, and time. Craig held that each GEM has as its neural substrate a large-scale network with the anterior insula cortex (AIC) serving as its central processing hub. This network integrates interoceptive signals that keep track of changes arising in the autonomic nervous system with hedonic and motivational signals based on the organism's sensory perception of its environment. Craig argued that GEMs function as moving windows of time within which \"a phenomenal self\" is experienced. By the \"phenomenal self,\" I mean a material, embodied self that forms an organism's subjective point of view on the world. Craig proposed what he called a \"cinemascopic\" theory of GEMs. GEMs are combined over time to form a stream of consciousness, which Craig compared to a movie, with each GEM corresponding to a single snapshot of this movie. I will argue that Craig's cinemascopic theory has implications for our understanding of what I will call the \"phenomenal now.\" There are three main theories of the phenomenal now in the philosophical literature. One point of contention between these theories is whether the phenomenal now has duration or temporal depth. I will argue that GEMs have duration and therefore count against so-called \"cinematic\" theories of the phenomenal now that take the contents of experience to be of discrete points or instances in time. However, there are different views within philosophy of how the phenomenal now can have duration. I end my chapter by considering how Craig's GEMs theory might bear on this debate.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"285-306"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the aftermath of psychological trauma, many individuals experience perturbations in interoception, a term that broadly references the ability to accurately detect body signals and integrate these signals with emotional states. These interoceptive disruptions can manifest in different ways, including blunting or amplification of sensitivity to internal physiological signals. In this chapter we review extant neurophysiological research on interoception in trauma-exposed populations, with a particular focus on the effects of chronic interpersonal trauma, such as childhood maltreatment and racial discrimination. We explore research that used different types of interoceptive assays, from self-report measures to electrophysiological and neuroimaging tools to characterize the disruptions in pain perception, interoceptive acuity, and physiological responses that may arise after a traumatic event. Finally, we discuss interventions that are designed to target interoceptive mechanisms, from exposure-based therapies to mindfulness-based practices, as well as future directions in trauma interoception research.
{"title":"The Neurophysiology of Interoceptive Disruptions in Trauma-Exposed Populations.","authors":"Negar Fani, Travis Fulton, Boris Botzanowski","doi":"10.1007/7854_2024_469","DOIUrl":"10.1007/7854_2024_469","url":null,"abstract":"<p><p>In the aftermath of psychological trauma, many individuals experience perturbations in interoception, a term that broadly references the ability to accurately detect body signals and integrate these signals with emotional states. These interoceptive disruptions can manifest in different ways, including blunting or amplification of sensitivity to internal physiological signals. In this chapter we review extant neurophysiological research on interoception in trauma-exposed populations, with a particular focus on the effects of chronic interpersonal trauma, such as childhood maltreatment and racial discrimination. We explore research that used different types of interoceptive assays, from self-report measures to electrophysiological and neuroimaging tools to characterize the disruptions in pain perception, interoceptive acuity, and physiological responses that may arise after a traumatic event. Finally, we discuss interventions that are designed to target interoceptive mechanisms, from exposure-based therapies to mindfulness-based practices, as well as future directions in trauma interoception research.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"217-244"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dissociative symptoms and disorders of dissociation are characterised by disturbances in the experience of the self and the surrounding world, manifesting as a breakdown in the normal integration of consciousness, memory, identity, emotion, and perception. This paper aims to provide insights into dissociative symptoms from the perspective of interoception, the sense of the body's internal physiological state, adopting a transdiagnostic framework.Dissociative symptoms are associated with a blunting of autonomic reactivity and a reduction in interoceptive precision. In addition to the central function of interoception in homeostasis, afferent visceral signals and their neural and mental representation have been shown to shape emotional feeling states, support memory encoding, and contribute to self-representation. Changes in interoceptive processing and disrupted integration of interoceptive signals into wider cognition may contribute to detachment from the body and the world, blunted emotional experience, and altered subjective recall, as experienced by individuals who suffer from dissociation.A better understanding of the role of altered interoceptive integration across the symptom areas of dissociation could thus provide insights into the neurophysiological mechanisms underlying dissociative disorders. As new therapeutic approaches targeting interoceptive processing emerge, recognising the significance of interoceptive mechanisms in dissociation holds potential implications for future treatment targets.
{"title":"Dissociative Symptoms and Interoceptive Integration.","authors":"Sascha P Woelk, Sarah N Garfinkel","doi":"10.1007/7854_2024_480","DOIUrl":"10.1007/7854_2024_480","url":null,"abstract":"<p><p>Dissociative symptoms and disorders of dissociation are characterised by disturbances in the experience of the self and the surrounding world, manifesting as a breakdown in the normal integration of consciousness, memory, identity, emotion, and perception. This paper aims to provide insights into dissociative symptoms from the perspective of interoception, the sense of the body's internal physiological state, adopting a transdiagnostic framework.Dissociative symptoms are associated with a blunting of autonomic reactivity and a reduction in interoceptive precision. In addition to the central function of interoception in homeostasis, afferent visceral signals and their neural and mental representation have been shown to shape emotional feeling states, support memory encoding, and contribute to self-representation. Changes in interoceptive processing and disrupted integration of interoceptive signals into wider cognition may contribute to detachment from the body and the world, blunted emotional experience, and altered subjective recall, as experienced by individuals who suffer from dissociation.A better understanding of the role of altered interoceptive integration across the symptom areas of dissociation could thus provide insights into the neurophysiological mechanisms underlying dissociative disorders. As new therapeutic approaches targeting interoceptive processing emerge, recognising the significance of interoceptive mechanisms in dissociation holds potential implications for future treatment targets.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"245-277"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140956751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katelyn I Oliver, Dasani DelRosario, Jennifer S Stevens
Although women are diagnosed with anxiety and stress-related disorders at twice the rate of men, there remains a lack of clarity around how to enhance treatment within each sex to reduce disparate rates of anxiety. However, in recent years, a growing literature has identified neural, cognitive, and physiological mechanisms that contribute to sex differences in fear and anxiety, with the promise of informing tailored treatment approaches. Here, we review recent findings, focusing on human studies among healthy populations as well as among patients with generalized anxiety, social anxiety disorder, post-traumatic stress disorder, and panic disorder. The literature reveals nuanced differences in the types of stimuli that preferentially evoke anxiety and stress responses in women and men, as well as sex differences in threat neurocircuitry that mediates the behavioral, physiological, and subjective components of fear and anxiety.
{"title":"Sex Differences in the Neurobiology of Fear and Anxiety.","authors":"Katelyn I Oliver, Dasani DelRosario, Jennifer S Stevens","doi":"10.1007/7854_2024_536","DOIUrl":"10.1007/7854_2024_536","url":null,"abstract":"<p><p>Although women are diagnosed with anxiety and stress-related disorders at twice the rate of men, there remains a lack of clarity around how to enhance treatment within each sex to reduce disparate rates of anxiety. However, in recent years, a growing literature has identified neural, cognitive, and physiological mechanisms that contribute to sex differences in fear and anxiety, with the promise of informing tailored treatment approaches. Here, we review recent findings, focusing on human studies among healthy populations as well as among patients with generalized anxiety, social anxiety disorder, post-traumatic stress disorder, and panic disorder. The literature reveals nuanced differences in the types of stimuli that preferentially evoke anxiety and stress responses in women and men, as well as sex differences in threat neurocircuitry that mediates the behavioral, physiological, and subjective components of fear and anxiety.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"377-404"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Antenatal mood disturbances are experienced by as many as 20% of pregnant mothers and are commonly treated with serotonin reuptake inhibitor (SRI) antidepressants. Both maternal depression and SRIs during pregnancy are associated with low birth weight and infant neurobehavioral disturbances, as well as longer-term impacts on child neurodevelopment, behavior, and mental health. As maternal depression and its pharmacotherapy are inherently interrelated prenatal exposures, distinguishing how these early life factors uniquely impact child development remains methodologically challenging. Over the past several years, however, advanced neuroimaging has been successfully used to identify neural correlates of prenatal depression and SRI antidepressant exposure on the developing brain, extending from the early newborn period through adolescence. In this review, we examine the use of magnetic resonance imaging and electroencephalography to study child brain structure or function, with a specific focus on prenatal antidepressants as the primary exposure in relation to either typical development or exposure to maternal depressed mood alone. We include both cross-sectional and longitudinal neuroimaging studies, as well as those that link early brain findings with cognitive or behavioral outcome in childhood. We also discuss factors that may shape neurodevelopmental risk (e.g., maternal mental illness severity, sex differences, genetic variability) and present suggestions for future research that will advance our understanding of child brain development in the context of maternal mood disturbances during pregnancy.
{"title":"Prenatal Antidepressant Exposure and the Developing Brain: A Review of Neuroimaging Findings.","authors":"Kayleigh S J Campbell, Tim F Oberlander","doi":"10.1007/7854_2025_591","DOIUrl":"10.1007/7854_2025_591","url":null,"abstract":"<p><p>Antenatal mood disturbances are experienced by as many as 20% of pregnant mothers and are commonly treated with serotonin reuptake inhibitor (SRI) antidepressants. Both maternal depression and SRIs during pregnancy are associated with low birth weight and infant neurobehavioral disturbances, as well as longer-term impacts on child neurodevelopment, behavior, and mental health. As maternal depression and its pharmacotherapy are inherently interrelated prenatal exposures, distinguishing how these early life factors uniquely impact child development remains methodologically challenging. Over the past several years, however, advanced neuroimaging has been successfully used to identify neural correlates of prenatal depression and SRI antidepressant exposure on the developing brain, extending from the early newborn period through adolescence. In this review, we examine the use of magnetic resonance imaging and electroencephalography to study child brain structure or function, with a specific focus on prenatal antidepressants as the primary exposure in relation to either typical development or exposure to maternal depressed mood alone. We include both cross-sectional and longitudinal neuroimaging studies, as well as those that link early brain findings with cognitive or behavioral outcome in childhood. We also discuss factors that may shape neurodevelopmental risk (e.g., maternal mental illness severity, sex differences, genetic variability) and present suggestions for future research that will advance our understanding of child brain development in the context of maternal mood disturbances during pregnancy.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"1-22"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alcohol is the most harmful drug of abuse, making alcoholism a major economic and public health crisis. Unsurprisingly, this has led to the majority of the neurobiological research on alcohol focusing on its direct effects on an individual, including those affected by foetal alcohol spectrum disorders (FASDs). However, research has shown that heavy paternal drinking predicts earlier and heavier adolescent drinking in the offspring, accompanied by other behavioural and molecular changes. While alcohol use disorder (AUD) is highly heritable, research on genetic variants alone does not sufficiently account for AUD risk and the FASDs-like symptoms seen in offspring of alcoholic fathers. Recently, there has been an increase in appreciation of the importance of epigenetic mechanisms of inheritance, which transfer changes due to parental experiences through the germline. This chapter aims to present an overview of the current knowledge on the inter- and transgenerational impacts of preconceptual paternal alcohol consumption (PPAC), the outcomes seen across generations and the mechanisms by which these changes may be passed down generations.
{"title":"Functional Consequences Paternal Preconceptual Alcohol Consumption.","authors":"Sahir Hussain, Darren Day, Bart Ellenbroek","doi":"10.1007/7854_2025_601","DOIUrl":"10.1007/7854_2025_601","url":null,"abstract":"<p><p>Alcohol is the most harmful drug of abuse, making alcoholism a major economic and public health crisis. Unsurprisingly, this has led to the majority of the neurobiological research on alcohol focusing on its direct effects on an individual, including those affected by foetal alcohol spectrum disorders (FASDs). However, research has shown that heavy paternal drinking predicts earlier and heavier adolescent drinking in the offspring, accompanied by other behavioural and molecular changes. While alcohol use disorder (AUD) is highly heritable, research on genetic variants alone does not sufficiently account for AUD risk and the FASDs-like symptoms seen in offspring of alcoholic fathers. Recently, there has been an increase in appreciation of the importance of epigenetic mechanisms of inheritance, which transfer changes due to parental experiences through the germline. This chapter aims to present an overview of the current knowledge on the inter- and transgenerational impacts of preconceptual paternal alcohol consumption (PPAC), the outcomes seen across generations and the mechanisms by which these changes may be passed down generations.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"117-147"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This chapter explores the insula's role in shaping body image through interoception - the neural process of sensing, interpreting, and integrating internal bodily signals to facilitate a coherent sense of self. Drawing on A.D. (Bud) Craig's hierarchical model, which emphasizes the insula's integration of sensory input into higher-order self-representations, we examine how disruptions in interoceptive processing may contribute to body image disturbance. This framework is applied to mental health conditions such as anorexia nervosa, body dysmorphic disorder, as well as physical health conditions including phantom limb pain and cancer, highlighting evidence for impaired interoceptive signaling and altered insular cortex function. We propose a mechanistic model describing how such disruptions can affect both sensory processing and the subjective experience of the body, leading to distorted body perception. We conclude with a discussion of future research directions and the potential for interoception-based therapeutic interventions targeting body image disturbance.
{"title":"Sensing the Self: The Role of the Insula and Interoception in Body Image.","authors":"Emily M Choquette, Sahib S Khalsa","doi":"10.1007/7854_2025_581","DOIUrl":"10.1007/7854_2025_581","url":null,"abstract":"<p><p>This chapter explores the insula's role in shaping body image through interoception - the neural process of sensing, interpreting, and integrating internal bodily signals to facilitate a coherent sense of self. Drawing on A.D. (Bud) Craig's hierarchical model, which emphasizes the insula's integration of sensory input into higher-order self-representations, we examine how disruptions in interoceptive processing may contribute to body image disturbance. This framework is applied to mental health conditions such as anorexia nervosa, body dysmorphic disorder, as well as physical health conditions including phantom limb pain and cancer, highlighting evidence for impaired interoceptive signaling and altered insular cortex function. We propose a mechanistic model describing how such disruptions can affect both sensory processing and the subjective experience of the body, leading to distorted body perception. We conclude with a discussion of future research directions and the potential for interoception-based therapeutic interventions targeting body image disturbance.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"107-125"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Deficits in memory, language, and other cognitive domains that impact an individual's ability to perform necessary tasks of daily living are symptoms of dementia, which is a major cause of death and disability in older adults. As the global population continues to age, deepening our understanding of dementia is crucial. Alzheimer's disease is the leading cause of dementia and accounts for between 60% and 80% of total dementia cases. Declines in episodic memory are considered a hallmark of Alzheimer's disease and occur early in disease progression. The cognitive effects of Alzheimer's disease differ from the cognitive changes expected in nonpathological or normal aging. While some cognitive changes are expected as a part of the aging processes, the declines in cognition associated with Alzheimer's disease are to a degree that the individual diagnosed with the disease is unable to function independently in activities of daily living. In this review, we will discuss how cognition is impacted by both normal and pathological aging, with a focus on Alzheimer's disease. We describe the progressive nature of Alzheimer's disease, as well as the effects of each stage of the disease on cognition.
{"title":"Cognitive Decline in Alzheimer's Disease.","authors":"Abigail A Testo, Gwenyth Roundy, Julie A Dumas","doi":"10.1007/7854_2024_527","DOIUrl":"10.1007/7854_2024_527","url":null,"abstract":"<p><p>Deficits in memory, language, and other cognitive domains that impact an individual's ability to perform necessary tasks of daily living are symptoms of dementia, which is a major cause of death and disability in older adults. As the global population continues to age, deepening our understanding of dementia is crucial. Alzheimer's disease is the leading cause of dementia and accounts for between 60% and 80% of total dementia cases. Declines in episodic memory are considered a hallmark of Alzheimer's disease and occur early in disease progression. The cognitive effects of Alzheimer's disease differ from the cognitive changes expected in nonpathological or normal aging. While some cognitive changes are expected as a part of the aging processes, the declines in cognition associated with Alzheimer's disease are to a degree that the individual diagnosed with the disease is unable to function independently in activities of daily living. In this review, we will discuss how cognition is impacted by both normal and pathological aging, with a focus on Alzheimer's disease. We describe the progressive nature of Alzheimer's disease, as well as the effects of each stage of the disease on cognition.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"181-195"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
An implicit tenet of the alcohol use disorder (AUD) research field is that knowledge of how alcohol interacts with the brain is critical to the development of an understanding of vulnerability to AUD and treatment approaches. Gaining this understanding requires the mapping of brain function critical to specific components of this heterogeneous disorder. Early approaches in humans and animal models focused on the determination of specific brain regions sensitive to alcohol action and their participation in AUD-relevant behaviors. Broadly speaking, this research has focused on three domains, Binge/Intoxication, Negative Affect/Withdrawal, and Preoccupation/Anticipation, with a number of regions identified as participating in each. With the generational advances in technologies that the field of neuroscience has undergone over the last two decades, this focus has shifted to a circuit-based analysis. A wealth of new data has sharpened the field's focus on the specific roles of the interconnectivity of multiple brain regions in AUD and AUD-relevant behaviors, as well as demonstrating that the three major domains described above have much fuzzier edges than originally thought.In this chapter, we very briefly review brain regions previously implicated in aspects of AUD-relevant behavior from animal model research. Next, we move to a more in-depth overview of circuit-based approaches, and the utilization of these approaches in current AUD research.
{"title":"Neural Circuitries and Alcohol Use Disorder: Cutting Corners in the Cycle.","authors":"Marie A Doyle, Anne Taylor, Danny G Winder","doi":"10.1007/7854_2023_454","DOIUrl":"10.1007/7854_2023_454","url":null,"abstract":"<p><p>An implicit tenet of the alcohol use disorder (AUD) research field is that knowledge of how alcohol interacts with the brain is critical to the development of an understanding of vulnerability to AUD and treatment approaches. Gaining this understanding requires the mapping of brain function critical to specific components of this heterogeneous disorder. Early approaches in humans and animal models focused on the determination of specific brain regions sensitive to alcohol action and their participation in AUD-relevant behaviors. Broadly speaking, this research has focused on three domains, Binge/Intoxication, Negative Affect/Withdrawal, and Preoccupation/Anticipation, with a number of regions identified as participating in each. With the generational advances in technologies that the field of neuroscience has undergone over the last two decades, this focus has shifted to a circuit-based analysis. A wealth of new data has sharpened the field's focus on the specific roles of the interconnectivity of multiple brain regions in AUD and AUD-relevant behaviors, as well as demonstrating that the three major domains described above have much fuzzier edges than originally thought.In this chapter, we very briefly review brain regions previously implicated in aspects of AUD-relevant behavior from animal model research. Next, we move to a more in-depth overview of circuit-based approaches, and the utilization of these approaches in current AUD research.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"379-399"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138800967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}