Biology of mood & anxiety disorders最新文献

{"title":"Genetic moderation of the association between regulatory focus and reward responsiveness: a proof-of-concept study.","authors":"Elena L Goetz,&nbsp;Ahmad R Hariri,&nbsp;Diego A Pizzagalli,&nbsp;Timothy J Strauman","doi":"10.1186/2045-5380-3-3","DOIUrl":"https://doi.org/10.1186/2045-5380-3-3","url":null,"abstract":"<p><strong>Unlabelled: </strong></p><p><strong>Background: </strong>Recent studies implicate individual differences in regulatory focus as contributing to self-regulatory dysfunction, particularly not responding to positive outcomes. How such individual differences emerge, however, is unclear. We conducted a proof-of-concept study to examine the moderating effects of genetically driven variation in dopamine signaling, a key modulator of neural reward circuits, on the association between regulatory focus and reward cue responsiveness.</p><p><strong>Method: </strong>Healthy Caucasians (N=59) completed a measure of chronic regulatory focus and a probabilistic reward task. A common functional genetic polymorphism impacting prefrontal dopamine signaling (COMT rs4680) was evaluated.</p><p><strong>Results: </strong>Response bias, the participants' propensity to modulate behavior as a function of reward, was predicted by an interaction of regulatory focus and COMT genotype. Specifically, self-perceived success at achieving promotion goals predicted total response bias, but only for individuals with the COMT genotype (Val/Val) associated with relatively increased phasic dopamine signaling and cognitive flexibility.</p><p><strong>Conclusions: </strong>The combination of success in promotion goal pursuit and Val/Val genotype appears to facilitate responding to reward opportunities in the environment. This study is among the first to integrate an assessment of self-regulatory style with an examination of genetic variability that underlies responsiveness to positive outcomes in goal pursuit.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"3 1","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2013-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-3-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31204543","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":"Considering trauma exposure in the context of genetics studies of posttraumatic stress disorder: a systematic review.","authors":"Julia Digangi, Guia Guffanti, Katie A McLaughlin, Karestan C Koenen","doi":"10.1186/2045-5380-3-2","DOIUrl":"10.1186/2045-5380-3-2","url":null,"abstract":"<p><strong>Background: </strong>Posttraumatic stress disorder (PTSD) is a debilitating anxiety disorder. Surveys of the general population suggest that while 50-85% of Americans will experience a traumatic event in their lifetime, only 2-50% will develop PTSD. Why some individuals develop PTSD following trauma exposure while others remain resilient is a central question in the field of trauma research. For more than half a century, the role of genetic influences on PTSD has been considered as a potential vulnerability factor. However, despite the exponential growth of molecular genetic studies over the past decade, limited progress has been made in identifying true genetic variants for PTSD.</p><p><strong>Methods: </strong>In an attempt to aid future genome wide association studies (GWAS), this paper presents a systematic review of 28 genetic association studies of PTSD. Inclusion criteria required that 1) all participants were exposed to Criterion A traumatic events, 2) polymorphisms of relevant genes were genotyped and assessed in relation to participants' PTSD status, 3) quantitative methods were used, and 4) articles were published in English and in peer-reviewed journals. In the examination of these 28 studies, particular attention was given to variables related to trauma exposure (e.g. number of traumas, type of trauma).</p><p><strong>Results: </strong>Results indicated that most articles did not report on the GxE interaction in the context of PTSD or present data on the main effects of E despite having data available. Furthermore, some studies that did consider the GxE interaction had significant findings, underscoring the importance of examining how genotypes can modify the effect of trauma on PTSD. Additionally, results indicated that only a small number of genes continue to be studied and that there were marked differences in methodologies across studies, which subsequently limited robust conclusions.</p><p><strong>Conclusions: </strong>As trauma exposure is a necessary condition for the PTSD diagnosis, this paper identifies gaps in the current literature as well as provides recommendations for how future GWAS studies can most effectively incorporate trauma exposure data in both the design and analysis phases of studies.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":" ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2013-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3598333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40204523","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":"Correction: Somatic therapies for treatment-resistant depression: ECT, TMS, VNS, DBS.","authors":"Cristina Cusin,&nbsp;Darin D Dougherty","doi":"10.1186/2045-5380-3-1","DOIUrl":"https://doi.org/10.1186/2045-5380-3-1","url":null,"abstract":"","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":" ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-3-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40200167","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":"Sleep quality and neural circuit function supporting emotion regulation.","authors":"Jared D Minkel,&nbsp;Kristin McNealy,&nbsp;Peter J Gianaros,&nbsp;Emily M Drabant,&nbsp;James J Gross,&nbsp;Stephen B Manuck,&nbsp;Ahmad R Hariri","doi":"10.1186/2045-5380-2-22","DOIUrl":"https://doi.org/10.1186/2045-5380-2-22","url":null,"abstract":"<p><strong>Unlabelled: </strong></p><p><strong>Background: </strong>Recent laboratory studies employing an extended sleep deprivation model have mapped sleep-related changes in behavior onto functional alterations in specific brain regions supporting emotion, suggesting possible biological mechanisms for an association between sleep difficulties and deficits in emotion regulation. However, it is not yet known if similar behavioral and neural changes are associated with the more modest variability in sleep observed in daily life.</p><p><strong>Methods: </strong>We examined relationships between sleep and neural circuitry of emotion using the Pittsburgh Sleep Quality Index and fMRI data from a widely used emotion regulation task focusing on cognitive reappraisal of negative emotional stimuli in an unselected sample of 97 adult volunteers (48 women; mean age 42.78±7.37 years, range 30-54 years old).</p><p><strong>Results: </strong>Emotion regulation was associated with greater activation in clusters located in the dorsomedial prefrontal cortex (dmPFC), left dorsolateral prefrontal cortex (dlPFC), and inferior parietal cortex. Only one subscale from the Pittsburgh Sleep Quality Index, use of sleep medications, was related to BOLD responses in the dmPFC and dlPFC during cognitive reappraisal. Use of sleep medications predicted lesser BOLD responses during reappraisal, but other aspects of sleep, including sleep duration and subjective sleep quality, were not related to neural activation in this paradigm.</p><p><strong>Conclusions: </strong>The relatively modest variability in sleep that is common in the general community is unlikely to cause significant disruption in neural circuits supporting reactivity or regulation by cognitive reappraisal of negative emotion. Use of sleep medication however, may influence emotion regulation circuitry, but additional studies are necessary to determine if such use plays a causal role in altering emotional responses.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"22"},"PeriodicalIF":0.0,"publicationDate":"2012-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-22","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31103989","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":"The relationship between Hippocampal asymmetry and working memory processing in combat-related PTSD - a monozygotic twin study.","authors":"Timothy Hall, Cherrie Galletly, C Richard Clark, Melinda Veltmeyer, Linda J Metzger, Mark W Gilbertson, Scott P Orr, Roger K Pitman, Alexander McFarlane","doi":"10.1186/2045-5380-2-21","DOIUrl":"10.1186/2045-5380-2-21","url":null,"abstract":"<p><strong>Unlabelled: </strong></p><p><strong>Background: </strong>PTSD is associated with reduction in hippocampal volume and abnormalities in hippocampal function. Hippocampal asymmetry has received less attention, but potentially could indicate lateralised differences in vulnerability to trauma. The P300 event-related potential component reflects the immediate processing of significant environmental stimuli and has generators in several brain regions including the hippocampus. P300 amplitude is generally reduced in people with PTSD.</p><p><strong>Methods: </strong>Our study examined hippocampal volume asymmetry and the relationship between hippocampal asymmetry and P300 amplitude in male monozygotic twins discordant for Vietnam combat exposure. Lateralised hippocampal volume and P300 data were obtained from 70 male participants, of whom 12 had PTSD. We were able to compare (1) combat veterans with current PTSD; (2) their non-combat-exposed co-twins; (3) combat veterans without current PTSD and (4) their non-combat-exposed co-twins.</p><p><strong>Results: </strong>There were no significant differences between groups in hippocampal asymmetry. There were no group differences in performance of an auditory oddball target detection task or in P300 amplitude. There was a significant positive correlation between P300 amplitude and the magnitude of hippocampal asymmetry in participants with PTSD.</p><p><strong>Conclusions: </strong>These findings suggest that greater hippocampal asymmetry in PTSD is associated with a need to allocate more attentional resources when processing significant environmental stimuli.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"21"},"PeriodicalIF":0.0,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31088861","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":"The role of the amygdala in the pathophysiology of panic disorder: evidence from neuroimaging studies.","authors":"Jieun E Kim,&nbsp;Stephen R Dager,&nbsp;In Kyoon Lyoo","doi":"10.1186/2045-5380-2-20","DOIUrl":"https://doi.org/10.1186/2045-5380-2-20","url":null,"abstract":"<p><p>Although the neurobiological mechanisms underlying panic disorder (PD) are not yet clearly understood, increasing amount of evidence from animal and human studies suggests that the amygdala, which plays a pivotal role in neural network of fear and anxiety, has an important role in the pathogenesis of PD. This article aims to (1) review the findings of structural, chemical, and functional neuroimaging studies on PD, (2) relate the amygdala to panic attacks and PD development, (3) discuss the possible causes of amygdalar abnormalities in PD, (4) and suggest directions for future research.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"20"},"PeriodicalIF":0.0,"publicationDate":"2012-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-20","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31063176","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":"Neural responses to threat and reward interact to predict stress-related problem drinking: A novel protective role of the amygdala.","authors":"Yuliya S Nikolova,&nbsp;Ahmad R Hariri","doi":"10.1186/2045-5380-2-19","DOIUrl":"https://doi.org/10.1186/2045-5380-2-19","url":null,"abstract":"<p><strong>Unlabelled: </strong></p><p><strong>Background: </strong>Research into neural mechanisms of drug abuse risk has focused on the role of dysfunction in neural circuits for reward. In contrast, few studies have examined the role of dysfunction in neural circuits of threat in mediating drug abuse risk. Although typically regarded as a risk factor for mood and anxiety disorders, threat-related amygdala reactivity may serve as a protective factor against substance use disorders, particularly in individuals with exaggerated responsiveness to reward.</p><p><strong>Findings: </strong>We used well-established neuroimaging paradigms to probe threat-related amygdala and reward-related ventral striatum reactivity in a sample of 200 young adult students from the ongoing Duke Neurogenetics Study. Recent life stress and problem drinking were assessed using self-report. We found a significant three-way interaction between threat-related amygdala reactivity, reward-related ventral striatum reactivity, and recent stress, wherein individuals with higher reward-related ventral striatum reactivity exhibit higher levels of problem drinking in the context of stress, but only if they also have lower threat-related amygdala reactivity. This three-way interaction predicted both contemporaneous problem drinking and problem drinking reported three-months later in a subset of participants.</p><p><strong>Conclusions: </strong>These findings suggest complex interactions between stress and neural responsiveness to both threat and reward mediate problem drinking. Furthermore, they highlight a novel protective role for threat-related amygdala reactivity against drug use in individuals with high neural reactivity to reward.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"19"},"PeriodicalIF":0.0,"publicationDate":"2012-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-19","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31047199","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":"Ankyrin 3: genetic association with bipolar disorder and relevance to disease pathophysiology.","authors":"Melanie P Leussis,&nbsp;Jon M Madison,&nbsp;Tracey L Petryshen","doi":"10.1186/2045-5380-2-18","DOIUrl":"https://doi.org/10.1186/2045-5380-2-18","url":null,"abstract":"<p><p> Bipolar disorder (BD) is a multi-factorial disorder caused by genetic and environmental influences. It has a large genetic component, with heritability estimated between 59-93%. Recent genome-wide association studies (GWAS) using large BD patient populations have identified a number of genes with strong statistical evidence for association with susceptibility for BD. Among the most significant and replicated genes is ankyrin 3 (ANK3), a large gene that encodes multiple isoforms of the ankyrin G protein. This article reviews the current evidence for genetic association of ANK3 with BD, followed by a comprehensive overview of the known biology of the ankyrin G protein, focusing on its neural functions and their potential relevance to BD. Ankyrin G is a scaffold protein that is known to have many essential functions in the brain, although the mechanism by which it contributes to BD is unknown. These functions include organizational roles for subcellular domains in neurons including the axon initial segment and nodes of Ranvier, through which ankyrin G orchestrates the localization of key ion channels and GABAergic presynaptic terminals, as well as creating a diffusion barrier that limits transport into the axon and helps define axo-dendritic polarity. Ankyrin G is postulated to have similar structural and organizational roles at synaptic terminals. Finally, ankyrin G is implicated in both neurogenesis and neuroprotection. ANK3 and other BD risk genes participate in some of the same biological pathways and neural processes that highlight several mechanisms by which they may contribute to BD pathophysiology. Biological investigation in cellular and animal model systems will be critical for elucidating the mechanism through which ANK3 confers risk of BD. This knowledge is expected to lead to a better understanding of the brain abnormalities contributing to BD symptoms, and to potentially identify new targets for treatment and intervention approaches.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"18"},"PeriodicalIF":0.0,"publicationDate":"2012-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-18","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30944363","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":"The genetic basis of mood and anxiety disorders - changing paradigms.","authors":"Elisabeth B Binder","doi":"10.1186/2045-5380-2-17","DOIUrl":"https://doi.org/10.1186/2045-5380-2-17","url":null,"abstract":"<p><p> Family, twin and epidemiologic studies all point to an important genetic contribution to the risk to develop mood and anxiety disorders. While some progress has been made in identifying relevant pathomechanisms for these disorders, candidate based strategies have often yielded controversial findings. Hopes were thus high when genome-wide genetic association studies became available and affordable and allowed a hypothesis-free approach to study genetic risk factors for these disorders. In an unprecendented scientific collaborative effort, large international consortia formed to allow the analysis of these genome-wide association datasets across thousands of cases and controls ([1] and see also http://www.broadinstitute.org/mpg/ricopili/). Now that large meta-analyses of genome-wide association studies (GWAS) have been published for bipolar disorder and major depression it has become clear that main effects of common variants are difficult to identify in these disorders, suggesting that additional approaches maybe needed to understand the genetic basis of these disorders [2,3].</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"17"},"PeriodicalIF":0.0,"publicationDate":"2012-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-17","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30942378","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":"Correlations between psychological tests and physiological responses during fear conditioning and renewal.","authors":"Karen G Martínez,&nbsp;Melissa Castro-Couch,&nbsp;José A Franco-Chaves,&nbsp;Brenda Ojeda-Arce,&nbsp;Gustavo Segura,&nbsp;Mohammed R Milad,&nbsp;Gregory J Quirk","doi":"10.1186/2045-5380-2-16","DOIUrl":"https://doi.org/10.1186/2045-5380-2-16","url":null,"abstract":"<p><strong>Unlabelled: </strong></p><p><strong>Background: </strong>Anxiety disorders are characterized by specific emotions, thoughts and physiological responses. Little is known, however, about the relationship between psychological/personality indices of anxiety responses to fear stimuli.</p><p><strong>Methods: </strong>We studied this relationship in healthy subjects by comparing scores on psychological and personality questionnaires with results of an experimental fear conditioning paradigm using a visual conditioned stimulus (CS). We measured skin conductance response (SCR) during habituation, conditioning, and extinction; subsequently testing for recall and renewal of fear 24 hours later.</p><p><strong>Results: </strong>We found that multiple regression models explained 45% of the variance during conditioning to the CS+, and 24% of the variance during renewal of fear to the CS+. Factors that explained conditioning included lower levels of conscientiousness, increased baseline reactivity (SCL), and response to the shock (UCR). Low levels of extraversion correlated with greater renewal. No model could be found to explain extinction learning or extinction recall to the CS+.</p><p><strong>Conclusions: </strong>The lack of correlation of fear extinction with personality and neuropsychological indices suggests that extinction may be less determined by trait variables and cognitive state, and may depend more on the subject's current emotional state. The negative correlation between fear renewal and extraversion suggests that this personality characteristic may protect against post-treatment relapse of symptoms of anxiety disorders.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"16"},"PeriodicalIF":0.0,"publicationDate":"2012-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-16","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30912553","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}