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Welcome to Biology of Mood & Anxiety Disorders
Ahmad R Hariri, Lisa M Shin
Biology of Mood & Anxiety Disorders , 2011, DOI: 10.1186/2045-5380-1-1
Abstract: Biology of Mood & Anxiety Disorders (BMAD) is a new open access peer-reviewed journal that publishes highly innovative basic, translational and clinical research that advances our understanding of mood and anxiety disorders. The journal welcomes research in all areas relevant to the disorders at the level of their underlying mechanisms. Research areas of interest include but are not limited to: pathophysiology, predictive risk markers, treatment predictors, individual differences and developmental trajectories of mood and anxiety disorders. Experimental approaches include but are not limited to: neuroimaging, psychophysiology, behavioral and molecular genetics, pharmacology, gene-environment interactions, and non-human animal models.Our idea behind BMAD is to create a venue for cutting-edge research that will become the destination of choice for the best work in the field. We are dedicated to providing an outlet for contributions that advance the field in any significant way. We believe that BMAD will be an important platform for presenting the findings of those interested in the biology of mood and anxiety disorders at any and all levels. The enthusiastic response from colleagues in neuroscience, psychology, psychiatry, psychophysiology, pharmacology and genetics who have graciously committed their time and expertise by joining the Editorial Board of BMAD [7] is testament to the value of this novel venue.Continued progress in understanding the biology of mood and anxiety disorders is critically dependent on the integration of knowledge gained across many disciplines, methodologies and model systems; currently such knowledge is divided across publications in many journals, none of which is focused entirely on the biology of mood and anxiety disorders. The Editors of BMAD thus believe that there is a need for a dedicated journal in this highly diverse field, and given the rising popularity of open access publication, we thought that a new open access journal in our f
The Melatonergic System in Mood and Anxiety Disorders and the Role of Agomelatine: Implications for Clinical Practice  [PDF]
Domenico De Berardis,Stefano Marini,Michele Fornaro,Venkataramanujam Srinivasan,Felice Iasevoli,Carmine Tomasetti,Alessandro Valchera,Giampaolo Perna,Maria-Antonia Quera-Salva,Giovanni Martinotti,Massimo di Giannantonio
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms140612458
Abstract: Melatonin exerts its actions through membrane MT1/MT2 melatonin receptors, which belong to the super family of G-protein-coupled receptors consisting of the typical seven transmembrane domains. MT1 and MT2 receptors are expressed in various tissues of the body either as single ones or together. A growing literature suggests that the melatonergic system may be involved in the pathophysiology of mood and anxiety disorders. In fact, some core symptoms of depression show disturbance of the circadian rhythm in their clinical expression, such as diurnal mood and other symptomatic variation, or are closely linked to circadian system functioning, such as sleep-wake cycle alterations. In addition, alterations have been described in the circadian rhythms of several biological markers in depressed patients. Therefore, there is interest in developing antidepressants that have a chronobiotic effect ( i.e., treatment of circadian rhythm disorders). As melatonin produces chronobiotic effects, efforts have been aimed at developing agomelatine, an antidepressant with melatonin agonist activity. The present paper reviews the role of the melatonergic system in the pathophysiology of mood and anxiety disorders and the clinical characteristics of agomelatine. Implications of agomelatine in “real world” clinical practice will be also discussed.
Signs of Mood and Anxiety Disorders in Chimpanzees  [PDF]
Hope R. Ferdowsian,Debra L. Durham,Charles Kimwele,Godelieve Kranendonk,Emily Otali,Timothy Akugizibwe,J. B. Mulcahy,Lilly Ajarova,Cassie Meré Johnson
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019855
Abstract: In humans, traumatic experiences are sometimes followed by psychiatric disorders. In chimpanzees, studies have demonstrated an association between traumatic events and the emergence of behavioral disturbances resembling posttraumatic stress disorder (PTSD) and depression. We addressed the following central question: Do chimpanzees develop posttraumatic symptoms, in the form of abnormal behaviors, which cluster into syndromes similar to those described in human mood and anxiety disorders?
Social Anxiety Disorder and Mood Disorders Comorbidity  [PDF]
Zerrin Binbay,Ahmet Koyuncu
Psikiyatride Guncel Yaklasimlar , 2012,
Abstract: Social Anxiety Disorder is a common disorder leading functional impairment. The comorbidity between mood disorders with social anxiety disorder is relatively common. This comorbidity impacts the clinical severity, resistance and functionality of patients. The systematic evaluation of the comorbidity in both patient groups should not be ignored and be carefully conducted. In general, social anxiety disorder starts at an earlier age than mood disorders and is reported to be predictor for subsequent major depression. The absence of comorbidity in patients with social anxiety disorder is a predictor of good response to treatment. In bipolar disorder patients with comorbid social anxiety disorder, there is an increased level of general psychopathology. Besides, they have poor outcome and increased risk of suicide. In this article, comorbidity between these two disorders has been evaluated in detail.
Therapygenetics: Using genetic markers to predict response to psychological treatment for mood and anxiety disorders  [cached]
Lester Kathryn J,Eley Thalia C
Biology of Mood & Anxiety Disorders , 2013, DOI: 10.1186/2045-5380-3-4
Abstract: Considerable variation is evident in response to psychological therapies for mood and anxiety disorders. Genetic factors alongside environmental variables and gene-environment interactions are implicated in the etiology of these disorders and it is plausible that these same factors may also be important in predicting individual differences in response to psychological treatment. In this article, we review the evidence that genetic variation influences psychological treatment outcomes with a primary focus on mood and anxiety disorders. Unlike most past work, which has considered prediction of response to pharmacotherapy, this article reviews recent work in the field of therapygenetics, namely the role of genes in predicting psychological treatment response. As this is a field in its infancy, methodological recommendations are made and opportunities for future research are identified.
Symptom Similarities and Differences in Anxiety and Depressive Disorders  [PDF]
Dilek Sirvanli Ozen,Elif Temizsu
Psikiyatride Guncel Yaklasimlar , 2010,
Abstract: The question if there is a valid distinction between depression and anxiety disorders remains controversial. These two disorders have various overlaps in the symptomatology and sometimes it is difficult to make a clear diagnosis. The difficulty in making a definite diagnosis destined researchers to determine the differences and the similarities between anxiety and depression. The negative affect which has multiple dimensions such as low self-esteem, negative mood and negative cognitions is seen as the common factor in both disorders. The positive affect which has been defined as the harmony and satisfaction with others and milieu, is regarded as the discriminating factor for the diagnosis of depression. Further research has characterized somatic arousal as the third dimension, a candidate to be the discriminating factor for anxiety disorders. Although phenotypic models appear to find a solution for this problem the facts that negative affect dimension is more loaded compared to the other two dimensions and predominance of negative affect on several symptom patterns prevent researchers to reach a conclusive results regarding the differences between these two disorders. In this review article, symptom similarities and differences of anxiety and depressive disorders are discussed within the frame of phenotypic models and some alternative ideas are provided for possible changes in upcoming versions of classification systems.
Anxiety and mood disorders in psychogenic nonepileptic seizures
Araújo Filho, Gerardo Maria de;Caboclo, Luís Otávio Sales Ferreira;
Journal of Epilepsy and Clinical Neurophysiology , 2007, DOI: 10.1590/S1676-26492007000500006
Abstract: the diagnosis of psychogenic nonepileptic seizures (pnes), particularly in patients with epilepsy, poses a special challenge to the physician in care of these patients. psychiatric disorders (pd) are more common among patients with epilepsy than in the general population, and this appears to be even more important in patients with pnes. depression and other mood disorders, as well as anxiety disorders - particularly panic attacks - may make the management of these patients even more difficult in the clinical practice. concomitant psychiatric conditions have been associated with a poor outcome in patients with pnes]. psychiatric and psychological intervention has been shown to be associated with improved outcome in pnes in outcome studies, although data is conflicting in this matter. the intricacies and practical implications of such issues are discussed.
Ghrelin's Roles in Stress, Mood, and Anxiety Regulation  [PDF]
Jen-Chieh Chuang,Jeffrey M. Zigman
International Journal of Peptides , 2010, DOI: 10.1155/2010/460549
Abstract: Several studies suggest that the peptide hormone ghrelin mediates some of the usual behavioral responses to acute and chronic stress. Circulating ghrelin levels have been found to rise following stress. It has been proposed that this elevated ghrelin helps animals cope with stress by generating antidepressant-like behavioral adaptations, although another study suggests that decreasing CNS ghrelin expression has antidepressant-like effects. Ghrelin also seems to have effects on anxiety, although these have been shown to be alternatively anxiogenic or anxiolytic. The current review discusses our current understanding of ghrelin's roles in stress, mood, and anxiety. 1. Introduction Metabolic syndrome and psychiatric disorders have become leading threats to the public health worldwide, and associations between the two now have been reported in several studies. For instance, a growing body of literature indicates that obesity is an important environmental risk factor for developing affective disorders. As an example, in a large cross sectional epidemiological U.S. study, a body mass index ≥ 30 was found to be associated with a 25% higher rate of mood disorders [1, 2]. Conversely, other studies suggest that psychological stress can increase the risk of developing obesity. For instance, a longitudinal study found that major depression in late adolescent girls was associated with a 2.3-fold increased risk of obesity in adulthood [3]. Also, a chart review of U.S. veterans with posttraumatic stress disorder showed a significantly increased rate of obesity [4]. Thus, it seems likely that certain circulating hormones and critical neuroanatomical circuits exist that regulate both energy homeostasis and our psychological state. Work from a handful of laboratories now suggests that the peptide hormone ghrelin is one such mediator of both behaviors linked to food intake and body weight and behaviors associated with psychosocial stress, mood, and anxiety. 2. Changes in Ghrelin Associated withPsychosocial Stress We and others have found that rises in ghrelin occur not only in response to states of energy insufficiency [5–8] but also following stress [9] (Figure 1). For example, elevations in either gastric ghrelin mRNA or total plasma ghrelin have been observed in response to various models of acute stress, including following a tail pinch stress protocol in ddy mice and following a water avoidance stress protocol in Wistar Kyoto and Sprague-Dawley rat [10, 11]. Also, rises in desacyl and acylated ghrelin plasma levels, preproghrelin mRNA levels, and numbers of ghrelin
The genetic basis of mood and anxiety disorders – changing paradigms
Binder Elisabeth B
Biology of Mood & Anxiety Disorders , 2012, DOI: 10.1186/2045-5380-2-17
Abstract: 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].
Effects of Acute MDMA Intoxication on Mood and Impulsivity: Role of the 5-HT2 and 5-HT1 Receptors  [PDF]
Janelle H. P. van Wel, Kim P. C. Kuypers, Eef L. Theunissen, Wendy M. Bosker, Katja Bakker, Johannes G. Ramaekers
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040187
Abstract: MDMA induces positive mood and increases impulse control during intoxication, but only a few studies on the neuropharmacological mechanisms underlying these processes have been conducted. It was hypothesized that pretreatment with 5-HT1 and 5-HT2 receptor blockers would prevent MDMA effects on mood and impulsivity. Subjects (N = 17) participated in a double-blind, placebo controlled, within-subject design involving 6 experimental conditions consisting of pretreatment (T1) and treatment (T2). T1 preceded T2 by 30 minutes. T1–T2 combinations were: placebo-placebo, 20 mg pindolol-placebo, 50 mg ketanserin-placebo, placebo-75 mg MDMA, 20 mg pindolol-75 mg MDMA and 50 mg ketanserin-75 g MDMA. Subjects completed a Profile of Mood States (POMS) questionnaire and several impulsivity tasks (Stop signal task, Matching familiar figures task, Cue dependent reversal learning task) at 1.5 hrs post-treatment. MDMA alone increased both positive (vigor, arousal, friendliness, elation, positive mood) and negative affect (anxiety, confusion) as assessed by the POMS questionnaire. MDMA also increased stop reaction time in the Stop signal task and reaction time in the Matching familiar figures task. Pretreatment with ketanserin blocked MDMA effects on positive affect, but not negative affect. Ketanserin did not influence the effects of MDMA on impulsivity. Pindolol did not interact with MDMA on any of the measures. In conclusion, 5-HT2 receptors mediate positive moods induced by MDMA but not negative moods or impulsivity. 5-HT1 receptors do not appear to be involved in MDMA effects on mood and impulse control. Trial Registration Nederlands Trial Register NTR2352
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