Current topics in behavioral neurosciences最新文献

{"title":"Correction to: Hearing Loss and Alzheimer Disease.","authors":"Arianna Di Stadio, Mickie J Hamiter, Dalila Roccamatisi, Anil K Lalwani","doi":"10.1007/978-3-031-84920-6_577","DOIUrl":"https://doi.org/10.1007/978-3-031-84920-6_577","url":null,"abstract":"","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":"69 ","pages":"C3"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069270","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":"New Approaches to Addiction Treatment Based on Learning and Memory.","authors":"Patrick Bach, Falk Kiefer","doi":"10.1007/7854_2023_457","DOIUrl":"10.1007/7854_2023_457","url":null,"abstract":"<p><p>Preclinical studies suggest that physiological learning processes are similar to changes observed in addiction at the molecular, neuronal and structural levels. Based on the importance of classical and instrumental conditioning in the development and maintenance of addictive disorders, many have suggested cue-exposure-based extinction training of conditioned, drug-related responses as a potential treatment of addiction. Recently, the development of virtual reality-assisted cue-exposure treatment has put forward new approaches to extinction training. Recent data indicated that it may also be possible to facilitate this extinction training through pharmacological interventions that strengthen memory consolidation during cue exposure. Another potential therapeutic intervention is based on the so-called reconsolidation theory. According to this hypothesis, already-consolidated memories return to a labile state when reactivated, allowing them to undergo another phase of consolidation - reconsolidation - which can be interfered with by pharmacological and behavioural interventions. These approaches suggest that the extinction of drug-related memories may represent a viable treatment strategy in the future treatment of addiction.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"689-717"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138800969","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":"Achieving Inclusion in Pharmacological Clinical Trials for Alzheimer's Disease.","authors":"Doris Molina-Henry, Rema Raman","doi":"10.1007/7854_2024_522","DOIUrl":"10.1007/7854_2024_522","url":null,"abstract":"<p><p>Participant recruitment and retention into randomized controlled trials (RCTs) is a growing and evolving science. It varies dramatically by discipline given the important and key choices that must be made based on the unique trial design considerations. In the field of Alzheimer's Disease (AD) therapeutics, recruitment goals, approaches, and strategies vary based on the disease stage of the target population which can range from asymptomatic adults with biomarker evidence of the disease to end-stage symptom management. This chapter discusses existing barriers and provides recommendations to achieve inclusive and timely recruitment in multi-center AD trials. It proposes an evidence-based recruitment framework anchored on culturally cognizant and participant focused study level and study site level efforts.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"229-242"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817629","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":"From Natural Behavior to Drug Screening: Invertebrates as Models to Study Mechanisms Associated with Alcohol Use Disorders.","authors":"Henrike Scholz","doi":"10.1007/7854_2022_413","DOIUrl":"10.1007/7854_2022_413","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Humans consume ethanol-containing beverages, which may cause an uncontrollable or difficult-to-control intake of ethanol-containing liquids and may result in alcohol use disorders. How the transition at the molecular level from \"normal\" ethanol-associated behaviors to addictive behaviors occurs is still unknown. One problem is that the components contributing to normal ethanol intake and their underlying molecular adaptations, especially in neurons that regulate behavior, are not clear. The fruit fly Drosophila melanogaster and the earthworm Caenorhabditis elegans show behavioral similarities to humans such as signs of intoxication, tolerance, and withdrawal. Underlying the phenotypic similarities, invertebrates and vertebrates share mechanistic similarities. For example in Drosophila melanogaster, the dopaminergic neurotransmitter system regulates the positive reinforcing properties of ethanol and in Caenorhabditis elegans, serotonergic neurons regulate feeding behavior. Since these mechanisms are fundamental molecular mechanisms and are highly conserved, invertebrates are good models for uncovering the basic principles of neuronal adaptation underlying the behavioral response to ethanol. This review will focus on the following aspects that might shed light on the mechanisms underlying normal ethanol-associated behaviors. First, the current status of what is required at the behavioral and cellular level to respond to naturally occurring levels of ethanol is summarized. Low levels of ethanol delay the development and activate compensatory mechanisms that in turn might be beneficial for some aspects of the animal's physiology. Repeated exposure to ethanol however might change brain structures involved in mediating learning and memory processes. The smell of ethanol is already a key component in the environment that is able to elicit behavioral changes and molecular programs. Minimal networks have been identified that regulate normal ethanol consumption. Other environmental factors that influence ethanol-induced behaviors include the diet, dietary supplements, and the microbiome. Second, the molecular mechanisms underlying neuronal adaptation to the cellular stressor ethanol are discussed. Components of the heat shock and oxidative stress pathways regulate adaptive responses to low levels of ethanol and in turn change behavior. The adaptive potential of the brain cells is challenged when the organism encounters additional cellular stressors caused by aging, endosymbionts or environmental toxins or excessive ethanol intake. Finally, to underline the conserved nature of these mechanisms between invertebrates and higher organisms, recent approaches to identify drug targets for ethanol-induced behaviors are provided. Already approved drugs regulate ethanol-induced behaviors and they do so in part by interfering with cellular stress pathways. In addition, invertebrates have been used to identify new compounds targeting molecules involved in the re","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"145-167"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10826796","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":"Alcohol-Induced Changes in Brain Microstructure: Uncovering Novel Pathophysiological Mechanisms of AUD Using Translational DTI in Humans and Rodents.","authors":"Wolfgang H Sommer, Santiago Canals","doi":"10.1007/7854_2025_585","DOIUrl":"10.1007/7854_2025_585","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) induces significant structural alterations in both gray and white matter, contributing to cognitive and functional impairments. This chapter presents a translational neuroimaging approach using diffusion-weighted MRI in humans and rodents to uncover novel pathophysiological mechanisms underlying AUD. Our studies demonstrate that increased mean diffusivity (MD) in gray matter reflects microglial reactivity and reduced extracellular space tortuosity, leading to enhanced volume neurotransmission. In white matter, fractional anisotropy (FA) reductions indicate progressive deterioration of key tracts, particularly the fimbria/fornix, linked to impaired cognitive flexibility. Importantly, longitudinal analyses reveal that white matter degeneration continues during early abstinence, suggesting that neuroinflammation and demyelination persist beyond alcohol cessation. Finally, we discuss how neuromodulatory interventions, such as transcranial magnetic stimulation (TMS), may promote recovery by enhancing myelin plasticity. These findings provide crucial insights into AUD's neurobiological underpinnings and highlight potential therapeutic targets for improving treatment outcomes.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"595-617"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990809","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":"Approach-Bias Retraining and Other Training Interventions as Add-On in the Treatment of AUD Patients.","authors":"Reinout W Wiers, Ting Pan, Pieter van Dessel, Mike Rinck, Johannes Lindenmeyer","doi":"10.1007/7854_2023_421","DOIUrl":"10.1007/7854_2023_421","url":null,"abstract":"<p><p>In the past two decades, a variety of cognitive training interventions have been developed to help people overcome their addictive behaviors. Conceptually, it is important to distinguish between programs in which reactions to addiction-relevant cues are trained (varieties of cognitive bias modification, CBM) and programs in which general abilities are trained such as working memory or mindfulness. CBM was first developed to study the hypothesized causal role in mental disorders: by directly manipulating the bias, it was investigated to what extent this influenced disorder-relevant behavior. In these proof-of-principle studies, the bias was temporarily modified in volunteers, either temporarily increased or decreased, with corresponding effects on behavior (e.g., beer consumption), in case the bias was successfully manipulated. In subsequent clinical randomized controlled trials (RCTs), training (away from the substance vs. sham training) was added to clinical treatment. These studies have demonstrated that CBM, as added to treatment, reduces relapse with a small effect of about 10% (similar effect size as for medication, with the strongest evidence for approach-bias modification). This has not been found for general ability training (e.g., working memory training), although effects on other psychological functions have been found (e.g., impulsivity). Mindfulness also has been found to help people overcome addictions, and different from CBM, also as stand-alone intervention. Research on (neuro-)cognitive mechanisms underlying approach-bias modification has pointed to a new perspective in which automatic inferences rather than associations are influenced by training, which has led to the development of a new variety of training: ABC training.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"641-687"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9511041","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 Relationship Between Oxytocin and Alcohol Dependence.","authors":"Jonas Schimmer, Ryan Patwell, Stephanie Küppers, Valery Grinevich","doi":"10.1007/7854_2023_444","DOIUrl":"10.1007/7854_2023_444","url":null,"abstract":"<p><p>The hypothalamic neuropeptide oxytocin (OT) is well known for its prosocial, anxiolytic, and ameliorating effects on various psychiatric conditions, including alcohol use disorder (AUD). In this chapter, we will first introduce the basic neurophysiology of the OT system and its interaction with other neuromodulatory and neurotransmitter systems in the brain. Next, we provide an overview over the current state of research examining the effects of acute and chronic alcohol exposure on the OT system as well as the effects of OT system manipulation on alcohol-related behaviors in rodents and humans. In rodent models of AUD, OT has been repeatedly shown to reduce ethanol consumption, particularly in models of acute alcohol exposure. In humans however, the results of OT administration on alcohol-related behaviors are promising but not yet conclusive. Therefore, we further discuss several physiological and methodological limitations to the effective application of OT in the clinic and how they may be mitigated by the application of synthetic OT receptor (OTR) agonists. Finally, we discuss the potential efficacy of cutting-edge pharmacology and gene therapies designed to specifically enhance endogenous OT release and thereby rescue deficient expression of OT in the brains of patients with severe forms of AUD and other incurable mental disorders.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"347-378"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10564281","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":"Modeling Brain Gene Expression in Alcohol Use Disorder with Genetic Animal Models.","authors":"Robert Hitzemann, Angela R Ozburn, Denesa Lockwood, Tamara J Phillips","doi":"10.1007/7854_2023_455","DOIUrl":"10.1007/7854_2023_455","url":null,"abstract":"<p><p>Animal genetic models have and will continue to provide important new information about the behavioral and physiological adaptations associated with alcohol use disorder (AUD). This chapter focuses on two models, ethanol preference and drinking in the dark (DID), their usefulness in interrogating brain gene expression data and the relevance of the data obtained to interpret AUD-related GWAS and TWAS studies. Both the animal and human data point to the importance for AUD of changes in synaptic transmission (particularly glutamate and GABA transmission), of changes in the extracellular matrix (specifically including collagens, cadherins and protocadherins) and of changes in neuroimmune processes. The implementation of new technologies (e.g., cell type-specific gene expression) is expected to further enhance the value of genetic animal models in understanding AUD.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"111-144"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11566292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138046591","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":"Involvement of Complement in Alzheimer's Disease: From Genetics Through Pathology to Therapeutic Strategies.","authors":"Nikoleta Daskoulidou, Sarah M Carpanini, Wioleta M Zelek, B Paul Morgan","doi":"10.1007/7854_2024_524","DOIUrl":"10.1007/7854_2024_524","url":null,"abstract":"<p><p>Complement is a critical component of innate immunity, evolved to defend against pathogens and clear toxic debris ranging from dead and dying cells to immune complexes. These roles make complement a key player in homeostasis; however, complement has a dark side. When the rigid control mechanisms fail, complement becomes dysregulated, acting as a driver of inflammation and resultant pathology in numerous diseases. Roles of complement in Alzheimer's disease (AD) and other dementias have emerged in recent years, supported by genetic, biomarker and pathological evidence and animal model studies. Numerous questions remain regarding the precise roles of complement in the brain in health and disease, including where and when complement is expressed, how it contributes to immune defence and garbage disposal in the healthy brain, and exactly how complement contributes to pathology in dementias. In this brief review, we will summarise current knowledge on complement roles in brain, present the evidence implicating complement in AD and explore whether complement represents an attractive therapeutic target for AD.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"3-24"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496925","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":"Correction to: Involvement of Complement in Alzheimer's Disease: From Genetics Through Pathology to Therapeutic Strategies.","authors":"Nikoleta Daskoulidou, Sarah M Carpanini, Wioleta M Zelek, B Paul Morgan","doi":"10.1007/7854_2024_576","DOIUrl":"10.1007/7854_2024_576","url":null,"abstract":"","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"C1"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028037","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}