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Biology of Mood & Anxiety Disorders

Jayne Morriss, Anastasia Christakou, Carien M van Reekum
BACKGROUND: Coordination of activity between the amygdala and ventromedial prefrontal cortex (vmPFC) is important for fear-extinction learning. Aberrant recruitment of this circuitry is associated with anxiety disorders. Here, we sought to determine if individual differences in future threat uncertainty sensitivity, a potential risk factor for anxiety disorders, underly compromised recruitment of fear extinction circuitry. Twenty-two healthy subjects completed a cued fear conditioning task with acquisition and extinction phases...
2015: Biology of Mood & Anxiety Disorders
Edward F Pace-Schott, Anne Germain, Mohammed R Milad
Post-traumatic stress disorder (PTSD) is accompanied by disturbed sleep and an impaired ability to learn and remember extinction of conditioned fear. Following a traumatic event, the full spectrum of PTSD symptoms typically requires several months to develop. During this time, sleep disturbances such as insomnia, nightmares, and fragmented rapid eye movement sleep predict later development of PTSD symptoms. Only a minority of individuals exposed to trauma go on to develop PTSD. We hypothesize that sleep disturbance resulting from an acute trauma, or predating the traumatic experience, may contribute to the etiology of PTSD...
2015: Biology of Mood & Anxiety Disorders
Elif A Duman, Turhan Canli
BACKGROUND: Previous research reported that individual differences in the stress response were moderated by an interaction between individuals' life stress experience and the serotonin transporter-linked polymorphic region (5-HTTLPR), a common polymorphism located in the promoter region of the serotonin transporter gene (SLC6A4). Furthermore, this work suggested that individual differences in SLC6A4 DNA methylation could be one underlying mechanism by which stressful life events might regulate gene expression...
2015: Biology of Mood & Anxiety Disorders
David M Schnyer, Christopher G Beevers, Megan T deBettencourt, Stephanie M Sherman, Jonathan D Cohen, Kenneth A Norman, Nicholas B Turk-Browne
There is growing interest in the use of neuroimaging for the direct treatment of mental illness. Here, we present a new framework for such treatment, neurocognitive therapeutics. What distinguishes neurocognitive therapeutics from prior approaches is the use of precise brain-decoding techniques within a real-time feedback system, in order to adapt treatment online and tailor feedback to individuals' needs. We report an initial feasibility study that uses this framework to alter negative attention bias in a small number of patients experiencing significant mood symptoms...
2015: Biology of Mood & Anxiety Disorders
M Justin Kim, Maital Neta, F Caroline Davis, Erika J Ruberry, Diana Dinescu, Todd F Heatherton, Mitchell A Stotland, Paul J Whalen
BACKGROUND: It has long been suggested that feedback signals from facial muscles influence emotional experience. The recent surge in use of botulinum toxin (BTX) to induce temporary muscle paralysis offers a unique opportunity to directly test this "facial feedback hypothesis." Previous research shows that the lack of facial muscle feedback due to BTX-induced paralysis influences subjective reports of emotional experience, as well as brain activity associated with the imitation of emotional facial expressions...
2014: Biology of Mood & Anxiety Disorders
Heide Klumpp, Michael K Keutmann, Daniel A Fitzgerald, Stewart A Shankman, K Luan Phan
BACKGROUND: Aberrant amygdala-prefrontal interactions at rest and during emotion processing are implicated in the pathophysiology of generalized social anxiety disorder (gSAD), a common disorder characterized by fears of potential scrutiny. Cognitive behavioral therapy (CBT) is first-line psychotherapy for gSAD and other anxiety disorders. While CBT is generally effective, there is a great deal of heterogeneity in treatment response. To date, predictors of success in CBT for gSAD include reduced amygdala reactivity and increased activity in prefrontal regulatory regions (e...
2014: Biology of Mood & Anxiety Disorders
Isabelle M Rosso, Elizabeth A Olson, Jennifer C Britton, S Evelyn Stewart, George Papadimitriou, William Ds Killgore, Nikos Makris, Sabine Wilhelm, Michael A Jenike, Scott L Rauch
BACKGROUND: Obsessive-compulsive disorder (OCD) is a common and debilitating neuropsychiatric illness thought to involve abnormal connectivity of widespread brain networks, including frontal-striatal-thalamic circuits. At least half of OCD cases arise in childhood and their underlying neuropathology may differ at least in part from that of adult-onset OCD. Yet, only a few studies have examined brain white matter (WM) integrity in childhood-onset OCD using diffusion tensor imaging (DTI), and none have examined potential associations with age at onset...
2014: Biology of Mood & Anxiety Disorders
Lisa L Hamm, Rachel H Jacobs, Meghan W Johnson, Daniel A Fitzgerald, Kate D Fitzgerald, Scott A Langenecker, Christopher S Monk, K Luan Phan
BACKGROUND: Childhood onset of anxiety disorders is associated with greater functional impairment and burden across the lifespan. Recent work suggests that generalized anxiety disorder (GAD) is characterized by dysfunctional connectivity in amygdala-based circuits at rest in adolescents, consistent with adults. However, neural mechanisms underlying a broad spectrum of often-comorbid anxiety disorders in children remains unclear and understudied. The current study examines amygdala functional connectivity at rest in children and adolescents across comorbid anxiety disorders (ADs) including youth with primary diagnoses of GAD and social phobia (SP)...
2014: Biology of Mood & Anxiety Disorders
Adam X Gorka, Jamie L Hanson, Spenser R Radtke, Ahmad R Hariri
BACKGROUND: The experience of early life stress is a consistently identified risk factor for the development of mood and anxiety disorders. Preclinical research employing animal models of early life stress has made inroads in understanding this association and suggests that the negative sequelae of early life stress may be mediated by developmental disruption of corticolimbic structures supporting stress responsiveness. Work in humans has corroborated this idea, as childhood adversity has been associated with alterations in gray matter volumes of the hippocampus, amygdala, and medial prefrontal cortex...
2014: Biology of Mood & Anxiety Disorders
Turhan Canli
In this article, I argue for a reconceptualization of major depressive disorder (major depression) as an infectious disease. I suggest that major depression may result from a parasitic, bacterial, or viral infection and present examples that illustrate possible pathways by which these microorganisms could contribute to the etiology of major depression. I also argue that the reconceptualization of the human body as an ecosystem for these microorganisms and the human genome as a host for non-human exogenous sequences may greatly amplify the opportunity to discover genetic links to the illness...
2014: Biology of Mood & Anxiety Disorders
Stephanie M Gorka, Brady D Nelson, K Luan Phan, Stewart A Shankman
BACKGROUND: Prior studies suggest that hyperactive insula responding to unpredictable aversiveness is a core feature of anxiety disorders. However, no study to date has investigated the neural correlates of unpredictable aversiveness in those with panic disorder (PD) with comorbid major depressive disorder (MDD). The aim of the current study was to examine group differences in neural responses to unpredictable and predictable aversiveness in 41 adults with either 1) current PD with comorbid MDD (PD-MDD), 2) current MDD with no lifetime diagnosis of an anxiety disorder (MDD-only), or 3) no lifetime diagnosis of psychopathology...
2014: Biology of Mood & Anxiety Disorders
Matthew D Sacchet, Gautam Prasad, Lara C Foland-Ross, Shantanu H Joshi, J Paul Hamilton, Paul M Thompson, Ian H Gotlib
BACKGROUND: Scientists are beginning to document abnormalities in white matter connectivity in major depressive disorder (MDD). Recent developments in diffusion-weighted image analyses, including tractography clustering methods, may yield improved characterization of these white matter abnormalities in MDD. In this study, we acquired diffusion-weighted imaging data from MDD participants and matched healthy controls. We analyzed these data using two tractography clustering methods: automated fiber quantification (AFQ) and the maximum density path (MDP) procedure...
2014: Biology of Mood & Anxiety Disorders
Erin L Maresh, Joseph P Allen, James A Coan
BACKGROUND: Social anxiety has been associated with potentiated negative affect and, more recently, with diminished positive affect. It is unclear how these alterations in negative and positive affect are represented neurally in socially anxious individuals and, further, whether they generalize to non-social stimuli. To explore this, we used a monetary incentive paradigm to explore the association between social anxiety and both the anticipation and consumption of non-social incentives...
2014: Biology of Mood & Anxiety Disorders
Stephanie Boehme, Alexander Mohr, Michael Pi Becker, Wolfgang Hr Miltner, Thomas Straube
BACKGROUND: Previous functional imaging studies using symptom provocation in patients with social anxiety disorder (SAD) reported inconsistent findings, which might be at least partially related to different time-dependent activation profiles in different brain areas. In the present functional magnetic resonance imaging study, we used a novel video-based symptom provocation design in order to investigate the magnitude and time course of activation in different brain areas in 20 SAD patients and 20 healthy controls...
2014: Biology of Mood & Anxiety Disorders
Liat Levita, Catherine Bois, Andrew Healey, Emily Smyllie, Evelina Papakonstantinou, Tom Hartley, Colin Lever
BACKGROUND: Animal studies have suggested that the hippocampus may play an important role in anxiety as part of the Behavioural Inhibition System (BIS), which mediates reactivity to threat and punishment and can predict an individual's response to anxiety-relevant cues in a given environment. The aim of the present structural magnetic resonance imaging (MRI) study was to examine the relationship between individual differences in BIS and hippocampal structure, since this has not received sufficient attention in non-clinical populations...
2014: Biology of Mood & Anxiety Disorders
Michael T Treadway, Diego A Pizzagalli
The neuroimaging literature of Major Depressive Disorder (MDD) has grown substantially over the last several decades, facilitating great advances in the identification of specific brain regions, neurotransmitter systems and networks associated with depressive illness. Despite this progress, fundamental questions remain about the pathophysiology and etiology of MDD. More importantly, this body of work has yet to directly influence clinical practice. It has long been a goal for the fields of clinical psychology and psychiatry to have a means of making objective diagnoses of mental disorders...
2014: Biology of Mood & Anxiety Disorders
Malin Gingnell, Victoria Ahlstedt, Elin Bannbers, Johan Wikström, Inger Sundström-Poromaa, Mats Fredrikson
BACKGROUND: Premenstrual dysphoric disorder (PMDD), characterized by luteal phase-induced negative affect and loss of impulse control, often results in compromised social interactions. Although amygdala activation is generally linked to negative affect, increased amygdala reactivity to aversive stimuli in the luteal phase has not been consistently reported in PMDD. We tested the hypothesis that amygdala hyper-reactivity in PMDD is symptom specific, rather than generalized, and linked to socially relevant stimuli...
2014: Biology of Mood & Anxiety Disorders
Christopher C Conway, George M Slavich, Constance Hammen
BACKGROUND: Recent studies examining the interaction between the 5-HTTLPR locus in the serotonin transporter gene and life stress in predicting depression have yielded equivocal results, leading some researchers to question whether 5-HTTLPR variation indeed regulates depressive responses to stress. Two possible sources of inconsistent data in this literature are imprecise stress assessment methodologies and a restricted focus on depression phenotypes as the outcome of interest, as opposed to transdiagnostic emotional symptoms such as internalizing and externalizing dimensions...
2014: Biology of Mood & Anxiety Disorders
Orna Issler, Roderick N Carter, Evan D Paul, Paul At Kelly, Henry J Olverman, Adi Neufeld-Cohen, Yael Kuperman, Christopher A Lowry, Jonathan R Seckl, Alon Chen, Pauline M Jamieson
BACKGROUND: Corticotropin-releasing factor type 2 receptors (CRFR2) are suggested to facilitate successful recovery from stress to maintain mental health. They are abundant in the midbrain raphe nuclei, where they regulate serotonergic neuronal activity and have been demonstrated to mediate behavioural consequences of stress. Here, we describe behavioural and serotonergic responses consistent with maladaptive recovery from stressful challenge in CRFR2-null mice. RESULTS: CRFR2-null mice showed similar anxiety levels to control mice before and immediately after acute restraint stress, and also after cessation of chronic stress...
2014: Biology of Mood & Anxiety Disorders
Michal Ziv, Philippe R Goldin, Hooria Jazaieri, Kevin S Hahn, James J Gross
BACKGROUND: Social anxiety disorder (SAD) is thought to involve deficits in emotion regulation, and more specifically, deficits in cognitive reappraisal. However, evidence for such deficits is mixed. METHODS: Using functional magnetic resonance imaging (fMRI) of blood oxygen-level dependent (BOLD) signal, we examined reappraisal-related behavioral and neural responses in 27 participants with generalized SAD and 27 healthy controls (HC) during three socio-emotional tasks: (1) looming harsh faces (Faces); (2) videotaped actors delivering social criticism (Criticism); and (3) written autobiographical negative self-beliefs (Beliefs)...
2013: Biology of Mood & Anxiety Disorders
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