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Depressive Phenotype (depressive + phenotype)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Interrelationship of childhood trauma, neuroticism, and depressive phenotype

DEPRESSION AND ANXIETY, Issue 3 2007
Valentina Moskvina Ph.D.
Abstract Both childhood trauma (CT) and genetic factors contribute to the pathophysiology of depression. We studied the relationship of CT to age of onset (AO) of depression, personality traits, and expression of symptom dimensions in 324 adults with recurrent unipolar depression. Subjects received structured psychiatric interviews and completed CT, depressive symptom, and personality rating questionnaires. Experience of at least one type of trauma was reported by 79.9% of subjects, and the most common forms of trauma were physical neglect, emotional abuse, and emotional neglect. There was an earlier AO of depression in the groups that reported CT compared to those that reported none, with earliest AO occurring in those who had experienced the highest levels of CT. There were no significant correlations between overall CT scores and neuroticism or extraversion. Total CT was a significant (P=.008) predictor of the Mood symptom dimension, mostly accounted for by emotional abuse (P=.019), and physical neglect predicted the Anxiety symptom dimension (P=.002). All types of CT are commonly reported in individuals with depression, and emotional abuse and physical neglect, though previously less well identified, appear to have an important role in the pathogenesis of depressive disorders. The effect of CT on individuals with an underlying genetic vulnerability to depression may result in differences in depressive phenotype characterized by earlier AO of depression and the expression of specific depressive symptom dimensions. Depression and Anxiety 24:163,168, 2007. © 2006 Wiley-Liss, Inc. [source]

The mood spectrum: improving the diagnosis of bipolar disorder

BIPOLAR DISORDERS, Issue 2005
Jules Angst
Although the distinction between bipolar and unipolar disorders served our field well in the early days of psychopharmacology, in clinical practice it is apparent that their phenotypes are only partially described by current diagnostic classification systems. A substantial body of evidence has accrued suggesting that clinical variability needs to be viewed in terms of a broad conceptualization of mood disorders and their common threshold or subthreshold comorbidity. The spectrum model provides a useful dimensional approach to psychopathology and is based on the assumption that early-onset and enduring symptoms shape the adult personality and establish a vulnerability to the subsequent development of Axis-I disorders. To obtain a clearer understanding of the depressive phenotype, it is pivotal that we increase our detection of hypomanic symptoms so that clinicians can better distinguish bipolar II disorder from unipolar depression. Diagnostic criteria sensitive to hypomanic symptoms have been identified that suggest bipolar II disorder is at least as prevalent as major depression. Moreover, the comorbidities of these illnesses are very different and alcoholism in particular appears to be a greater problem in bipolar II disorder than in unipolar depression. Structured clinical interviews and patient self-report questionnaires have also successfully identified the presence of hypomanic symptoms in patients with unipolar disorder and support the concept of a spectrum of bipolar illness. In conclusion, the importance of subthreshold syndromes should not be underestimated as failure to recognize bipolar spectrum disorder could delay treatment and worsen prognosis. [source]

Open questions in current models of antidepressant action

BRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2010
A Tanti
Research on depression and antidepressant drugs is necessary, as many patients display poor response to therapy. Different symptomatic and pathophysiological features have been proposed as end points of the depressive phenotype and of the antidepressant action, including anhedonia, depressed mood, alterations in morphology and activity of some brain areas (amygdala, nucleus accumbens, hippocampus, prefrontal cortex and cingulate cortex), modifications in the connectivity between brain structures, changes in neurotransmitters (serotonin, noradrenaline, glutamate and neuropeptides), brain plasticity (neurogenesis, neurotrophins) and abnormal function of the hypothalamic-pituitary adrenal axis. However, few models have been proposed to describe how these end points could induce the depressive phenotype and are involved in the mechanism of action of antidepressants. Here we propose a connectionist-inspired network of depression and antidepressant action, in which the different aetiological factors participating in the release of a depressive episode are represented by input nodes, the different symptomatic as well as pathophysiological end points are represented by an intermediate layer, and the onset of depression or of comorbid disease is represented by the output node. The occurrence of depression and the mechanism of the antidepressant action thus depend upon the weight of the interactions between the different end points, none of them being per se crucial to the onset of a depressive phenotype or to the antidepressant action. This model is heuristic to draw future lines of research concerning new antidepressant therapies, designing new animal models of depression and for a better understanding of the depressive pathology and of its comorbid pathology such as anxiety disorders. [source]