Current topics in behavioral neurosciences最新文献

{"title":"Biological Sex Disparities in Alzheimer's Disease.","authors":"Jawza A Almutairi, Emma J Kidd","doi":"10.1007/7854_2024_545","DOIUrl":"10.1007/7854_2024_545","url":null,"abstract":"<p><p>Alzheimer's disease is a highly complex and multifactorial neurodegenerative disorder, with age being the most significant risk factor. The incidence of Alzheimer's disease doubles every 5 years after the age of 65. Consequently, one of the major challenges in Alzheimer's disease research is understanding how the brain changes with age. Gaining insights into these changes could help identify individuals who are more prone to developing Alzheimer's disease as they age. Over the past 25 years, studies on brain aging have examined thousands of human brains to explore the neuronal basis of age-related cognitive decline. However, most of these studies have focused on adults over 60, often neglecting the critical menopause transition period. During menopause, women experience a substantial decline in ovarian sex hormone production, with a decrease of about 90% in estrogen levels. Estrogen is known for its neuroprotective effects, and its significant loss during menopause affects various biological systems, including the brain. Importantly, despite known differences in dementia risk between sexes, the impact of biological sex and sex hormones on brain aging and the development of Alzheimer's disease remains underexplored.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"79-104"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562395","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}

{"title":"Understanding Alcohol Consumption and Its Antecedents and Consequences in Daily Life: The Why and the How.","authors":"Dominic Reichert, Sarah Brüßler, Markus Reichert, Ulrich Ebner-Priemer","doi":"10.1007/7854_2024_486","DOIUrl":"10.1007/7854_2024_486","url":null,"abstract":"<p><p>Most of the scientific research on alcohol consumption behavior in humans is laboratory-based, as reflected by the ratio of laboratory vs. real-life contributions to this handbook. Studies in daily life, although having a long history in addiction research (Shiffman et al., Ann Behav Med 16:203-209, 1994), are in the minority. This is surprising, given that patients with substance use disorders are suffering in daily life and not in the laboratory setting. In other words, drinking patterns and symptoms of alcohol use disorder evolve not in the lab but in daily life, where patients show difficulties in limiting their alcohol intake accompanied with all kinds of related problems. The ultimate goal of all interventions, independent of being tailored toward restricted drinking or abstinence, is again an altered behavior in real life. Translated to practice, patients' behavior in the lab may not translate to daily life, often showing minimal ecological validity. Therefore, we have to question to which degree lab-based research findings translate into daily life. Fortunately, the current digital revolution provided us with more and more tools, enabling us to monitor, analyze, and change behavior in human everyday life. Our chapter does not intend to give a comprehensive overview of the daily life research on alcohol consumption over the last few decades as others do (Morgenstern et al., Alcohol Res Curr Rev 36:109, 2014; Piasecki, Alcohol Clin Exp Res 43:564-577, 2019; Shiffman, Psychol Asses 21:486-497, 2009; Votaw and Witkiewitz, Clin Psychol Sci 9:535-562, 2021; Wray et al., Alcohol Res Curr Rev 36:19-27, 2014). Instead, we aim at the following: first, to highlight the key advantages of ecological momentary assessment to motivate scientists to add daily life research components to their laboratory research and, second, to provide some guidance on how to begin with daily life research.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"453-474"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855130","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}

{"title":"Role of Metabolism on Alcohol Preference, Addiction, and Treatment.","authors":"María Elena Quintanilla, Yedy Israel","doi":"10.1007/7854_2023_422","DOIUrl":"10.1007/7854_2023_422","url":null,"abstract":"<p><p>Studies presented in this chapter show that: (1) in the brain, ethanol is metabolized by catalase to acetaldehyde, which condenses with dopamine forming salsolinol; (2) acetaldehyde-derived salsolinol increases the release of dopamine mediating, via opioid receptors, the reinforcing effects of ethanol during the acquisition of ethanol consumption, while (3) brain acetaldehyde does not influence the maintenance of chronic ethanol intake, it is suggested that a learned cue-induced hyperglutamatergic system takes precedence over the dopaminergic system. However, (4) following a prolonged ethanol deprivation, the generation of acetaldehyde in the brain again plays a role, contributing to the increase in ethanol intake observed during ethanol re-access, called the alcohol deprivation effect (ADE), a model of relapse behavior; (5) naltrexone inhibits the high ethanol intake seen in the ADE condition, suggesting that acetaldehyde-derived salsolinol via opioid receptors also contributes to the relapse-like drinking behavior. The reader is referred to glutamate-mediated mechanisms that trigger the cue-associated alcohol-seeking and that also contribute to triggering relapse.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"193-216"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9511038","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}

{"title":"Theoretical Frameworks and Mechanistic Aspects of Alcohol Addiction: Alcohol Addiction as a Reward Deficit/Stress Surfeit Disorder.","authors":"George F Koob, Leandro Vendruscolo","doi":"10.1007/7854_2023_424","DOIUrl":"10.1007/7854_2023_424","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) can be defined by a compulsion to seek and take alcohol, the loss of control in limiting intake, and the emergence of a negative emotional state when access to alcohol is prevented. Alcohol use disorder impacts multiple motivational mechanisms and can be conceptualized as a disorder that includes a progression from impulsivity (positive reinforcement) to compulsivity (negative reinforcement). Compulsive drug seeking that is associated with AUD can be derived from multiple neuroadaptations, but the thesis argued herein is that a key component involves the construct of negative reinforcement. Negative reinforcement is defined as drug taking that alleviates a negative emotional state. The negative emotional state that drives such negative reinforcement is hypothesized to derive from the dysregulation of specific neurochemical elements that are involved in reward and stress within basal forebrain structures that involve the ventral striatum and extended amygdala, respectively. Specific neurochemical elements in these structures include decreases in reward neurotransmission (e.g., decreases in dopamine and opioid peptide function in the ventral striatum) and the recruitment of brain stress systems (e.g., corticotropin-releasing factor [CRF]) in the extended amygdala, which contributes to hyperkatifeia and greater alcohol intake that is associated with dependence. Glucocorticoids and mineralocorticoids may play a role in sensitizing the extended amygdala CRF system. Other components of brain stress systems in the extended amygdala that may contribute to the negative motivational state of withdrawal include norepinephrine in the bed nucleus of the stria terminalis, dynorphin in the nucleus accumbens, hypocretin and vasopressin in the central nucleus of the amygdala, and neuroimmune modulation. Decreases in the activity of neuropeptide Y, nociception, endocannabinoids, and oxytocin in the extended amygdala may also contribute to hyperkatifeia that is associated with alcohol withdrawal. Such dysregulation of emotional processing may also significantly contribute to pain that is associated with alcohol withdrawal and negative urgency (i.e., impulsivity that is associated with hyperkatifeia during hyperkatifeia). Thus, an overactive brain stress response system is hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence, and to contribute to the compulsivity of AUD. The combination of the loss of reward function and recruitment of brain stress systems provides a powerful neurochemical basis for a negative emotional state that is responsible for the negative reinforcement that at least partially drives the compulsivity of AUD.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"17-77"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10138309","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}

{"title":"The Contribution of the Renin-Angiotensin System to Alzheimer's Disease.","authors":"Özge Güzel, Patrick G Kehoe","doi":"10.1007/7854_2024_525","DOIUrl":"10.1007/7854_2024_525","url":null,"abstract":"<p><p>The renin-angiotensin system (RAS) is becoming increasingly recognised as a biochemical pathway relevant to the development and progression of Alzheimer's disease (AD). RAS involvement in AD was initially linked to AD via numerous genetic association studies and more recent Genome-Wide Association Studies (GWAS), and in some cases in relation to classical hallmarks of AD pathology. Since these initial findings, which will be summarised here, several complementary areas of research are converging in support of what has been proposed as the Angiotensin Hypothesis for Alzheimer's disease. This hypothesis proposes how the RAS and disease-associated changes to the normal balance between opposing regulatory pathways within RAS warrant careful consideration in the pathogenesis of AD and its pathology. We discuss some of these in relation to RAS-targeting therapeutics, originally developed for the treatment of cardiovascular conditions, and how they might be repurposed as interventions for AD.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"107-127"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616634","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}

{"title":"Laboratory and Real-World Experimental Approaches to Understanding Alcohol Relapse.","authors":"Verica Milivojevic, Rajita Sinha","doi":"10.1007/7854_2023_456","DOIUrl":"10.1007/7854_2023_456","url":null,"abstract":"<p><p>Alcohol use disorder is highly prevalent and high risk of relapse remains a significant treatment challenge. Therefore, the utility of human laboratory models of relapse to further the understanding of psychobiological mechanisms that precipitate relapse risk and allow testing of novel interventions could be of benefit in expediting the development of effective treatments to target high relapse risk. Stress is a risk factor for the development of AUD and for relapse, and furthermore, chronic alcohol use leads to adaptations in central and peripheral stress biology. Here, we review our efforts to assess the integrity of these stress pathways in individuals with alcohol use disorder and whether adaptations in these systems play a role in relapse risk. Using validated human laboratory procedures to model two of the most common situations that contribute to relapse risk, namely stress and alcohol cues, we review how such models in the laboratory can predict subsequent relapse, and how we can measure specific identified biobehavioral markers of relapse effectively and ecologically in the real world. Finally, we discuss the significant implications of these findings for the development of novel and effective interventions that target stress dysregulation and craving as risk factors to treatment.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"427-451"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138175873","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}

{"title":"Role of the Microbiome and the Gut-Brain Axis in Alcohol Use Disorder: Potential Implication for Treatment Development.","authors":"Sophie Leclercq, Philippe de Timary","doi":"10.1007/7854_2024_478","DOIUrl":"10.1007/7854_2024_478","url":null,"abstract":"<p><p>The gut microbiota is constituted by trillions of microorganisms colonizing the human intestine. Studies conducted in patients with alcohol use disorder (AUD) have shown altered microbial composition related to bacteria, viruses, and fungi.This review describes the communication pathways between the gut and the brain, including the ones related to the bacterial metabolites, the inflammatory cytokines, and the vagus nerve. We described in more detail the gut-derived metabolites that have been shown to be implicated in AUD or that could potentially be involved in the development of AUD due to their immune and/or neuroactive properties, including tryptophan-derivatives, tyrosine-derivatives, short chain fatty acids.Finally, we discussed the potential beneficial effects of microbiome-based therapies for AUD such as probiotics, prebiotics, postbiotic, and phage therapy.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"737-754"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141445828","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}

{"title":"Understanding How Acute Alcohol Impacts Neural Encoding in the Rodent Brain.","authors":"Christopher C Lapish","doi":"10.1007/7854_2024_479","DOIUrl":"10.1007/7854_2024_479","url":null,"abstract":"<p><p>Alcohol impacts neural circuitry throughout the brain and has wide-ranging effects on the biophysical properties of neurons in these circuits. Articulating how these wide-ranging effects might eventually result in altered computational properties has the potential to provide a tractable working model of how alcohol alters neural encoding. This chapter reviews what is currently known about how acute alcohol influences neural activity in cortical, hippocampal, and dopaminergic circuits as these have been the primary focus of understanding how alcohol alters neural computation. While other neural systems have been the focus of exhaustive work on this topic, these brain regions are the ones where in vivo neural recordings are available, thus optimally suited to make the link between changes in neural activity and behavior. Rodent models have been key in developing an understanding of how alcohol impacts the function of these circuits, and this chapter therefore focuses on work from mice and rats. While progress has been made, it is critical to understand the challenges and caveats associated with experimental procedures, especially when performed in vivo, which are designed to answer this question and if/how to translate these data to humans. The hypothesis is discussed that alcohol impairs the ability of neural circuits to acquire states of neural activity that are transiently elevated and characterized by increased complexity. It is hypothesized that these changes are distinct from the traditional view of alcohol being a depressant of neural activity in the forebrain.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"401-423"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12284808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300336","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}

{"title":"Emotion Regulation Under Stress: A Social Processing and Memory Perspective.","authors":"Nicholas J Dennis, Tasha Bulgin, Casey M Nicastri, Cassandra Bell, Mauricio R Delgado","doi":"10.1007/7854_2024_560","DOIUrl":"https://doi.org/10.1007/7854_2024_560","url":null,"abstract":"<p><p>Research on emotion regulation often focuses on cognitively effortful self-regulation strategies, but exposure to stress has been shown to interfere with the underlying mechanisms supporting such processes. Understanding alternative strategies that potentially bolster emotion regulation under stress is an important topic of investigation. Two potential alternatives involve everyday occurrences of social processing and memory recall. Social support and past emotional experiences may help in guiding us toward appropriate neurophysiological responses through overlapping circuitry with stress and reward systems, while also buttressing cognitive regulation strategies by expanding one's perspective and allowing multiple opportunities to regulate retrospectively. In recognition that ongoing social and emotional events are often at the beginning of a cascade of both emotion regulation and memory processes, this chapter focuses on the emerging role of social relationships and autobiographical memory recall in regulating emotions under stress, highlighting opportunities and challenges associated with this process.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909591","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}

{"title":"Insights into the Neurobiology of Behavioral Inhibition from Nonhuman Primate Models.","authors":"Lillian J Campos, Carly M Drzewiecki, Andrew S Fox","doi":"10.1007/7854_2024_561","DOIUrl":"https://doi.org/10.1007/7854_2024_561","url":null,"abstract":"<p><p>Children with extreme behavioral inhibition (BI) are at a significantly greater risk to develop anxiety disorders later in life. We and others have identified similar early-life temperamental BI in nonhuman primates (NHPs), including rhesus monkeys. NHP models of BI provide a unique opportunity to study the neurobiology of BI in a species that shares biological, developmental, and socioemotional similarities with humans. Rhesus monkey models have identified a distributed brain circuit that includes the central extended amygdala (EAc) as being critical for the genesis of BI. By leveraging multimodal neuroimaging, brain lesions, RNA-sequencing, and viral vector manipulations in rhesus monkeys, these studies have identified specific brain regions, genetic factors, and molecular mechanisms that causally contribute to BI. Here, we discuss these findings from NHPs and how they fit into a translational framework that can contribute to our understanding of the neural circuits that give rise to the risk to develop anxiety and depressive disorders.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909593","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}