Precipitation Of Depression Research Articles

Beyond New Neurons in the Adult Hippocampus: Imipramine Acts as a Pro-Astrogliogenic Factor and Rescues Cognitive Impairments Induced by Stress Exposure.

Depression is a prevalent, socially burdensome disease. Different studies have demonstrated the important role of astrocytes in the pathophysiology of depression as modulators of neurotransmission and neurovascular coupling. This is evidenced by astrocyte impairments observed in brains of depressed patients and the appearance of depressive-like behaviors upon astrocytic dysfunctions in animal models. However, little is known about the importance of de novo generated astrocytes in the mammalian brain and in particular its possible involvement in the precipitation of depression and in the therapeutic actions of current antidepressants (ADs). Therefore, we studied the modulation of astrocytes and adult astrogliogenesis in the hippocampal dentate gyrus (DG) of rats exposed to an unpredictable chronic mild stress (uCMS) protocol, untreated and treated for two weeks with antidepressants—fluoxetine and imipramine. Our results show that adult astrogliogenesis in the DG is modulated by stress and imipramine. This study reveals that distinct classes of ADs impact differently in the astrogliogenic process, showing different cellular mechanisms relevant to the recovery from behavioral deficits induced by chronic stress exposure. As such, in addition to those resident, the newborn astrocytes in the hippocampal DG might also be promising therapeutic targets for future therapies in the neuropsychiatric field.

Healing the Wounded Self: Combining Hypnotherapy With Ego State Therapy

The purpose of this article is to formulate a theoretical conceptualization for utilizing ego state therapy (EST) as an adjunct with cognitive hypnotherapy (CH) for depression. As the relationship between life events and onset of depression is very complex, it is not clear from current literature how stressors cause depressive symptoms. The notion of “wounded self,” derived from the work of Wolfe (2005, 2006), is examined as a potential unifying concept for binding the role of risk factors in the precipitation of depression. By incorporating wounded self, the circular feedback model of depression, on which CH for depression is based, is expanded. This revised version provides conceptual and empirical underpinnings for integrating EST with CH in the management of depression.

Adaptation of an internet-based depression prevention intervention for Chinese adolescents: from “CATCH-IT” to “grasp the opportunity”

There is a dearth of information on the compatibility of Western-developed, internet-based interventions that prevent onset and precipitation of depression in global settings. Recently, Project CATCH-IT (Competent Adulthood Transition with Cognitive-behavioral, Humanistic and Interpersonal Training), an information technology-based intervention, was adapted to prevent depression in Hong Kong Chinese adolescents. This paper evaluates qualitative data from consultations to develop a revised intervention of CATCH-IT for Hong Kong youth. A theoretical thematic analysis approach was used to analyze data. Materials from three consultation trips which included focus groups (2007), an expert panel (2007), a public health campaign (2009), and a joint primary care physician-social worker review group (2010) were compiled. Authors (KS and AZ) independently reviewed the data and applied the theoretical framework of behavioral vaccines to code the data. These data were subsequently consolidated to provide a coherent narrative analysis. The cognitive behavioral therapy (CBT), behavioral activation (BA), and resiliency modules were maintained, while the interpersonal therapy (IPT) modules of CATCH-IT were excluded in the Hong Kong adaptation. Concurrent self-reports of drinking, smoking, illicit drug use and gambling behavior were added. Rather than primary care consultations, social worker consultations may be the best point of entry for intervention. Socio-cultural relevance of psychotherapeutics and delivery context of internet-based interventions will require significant adaptation for the Hong Kong setting. However, because of community engagement throughout the process of adaptation, we believe the CATCH-IT intervention can be adapted for Chinese adolescents in Hong Kong with retained fidelity. The revised intervention is called "Grasp the Opportunity".

The Pro-inflammatory Cytokine TNF-α Regulates the Activity and Expression of the Serotonin Transporter (SERT) in Astrocytes

Pro-inflammatory cytokines have been implicated in the precipitation of depression and related disorders, and the antidepressant sensitive serotonin transporter (SERT) may be a major target for immune regulation in these disorders. Here, we focus on astrocytes, a major class of immune competent cells in the brain, to examine the effects of pro-longed treatment with tumor necrosis factor-alpha (TNF-α) on SERT activity. We first established that high-affinity serotonin uptake into C6 glioma cells occurs through a SERT-dependent mechanism. Functional SERT expression is also confirmed for primary astrocytes. In both cell types, exposure to TNF-α resulted in a dose- and time-dependent increase in SERT-mediated 5-HT uptake, which was sustained for at least 48h post-stimulation. Further analysis in primary astrocytes revealed that TNF-α enhanced the transport capacity (Vmax) of SERT-specific 5-HT uptake, suggesting enhanced transporter expression, consistent with our observation of an increase in SERT mRNA levels. We confirmed that in both, primary astrocytes and C6 glioma cells, treatment with TNF-α activates the p38 mitogen-activated protein kinase (MAPK) signaling pathway. Pre-treatment with the p38 MAPK inhibitor SB203580 attenuated the TNF-α mediated stimulation of 5-HT transport in both, C6 glioma and primary astrocytes. In summary, we show that SERT gene expression and activity in astrocytes is subject to regulation by TNF-α, an effect that is at least in part dependent on p38 MAPK activation.

From psychoanalysis to epidemiology: autobiographical notes

From psychoanalysis to epidemiology: autobiographical notes

Prediction of medium-term outcome by cortisol response to the combined dexamethasone-CRH test in patients with remitted depression.

Current hypotheses hold that mechanisms underlying abnormal hypothalamic-pituitary-adrenocortical (HPA) function are causal factors in the precipitation of depression. If this is the case, then normalization of initially disturbed HPA regulation should indicate a good prognosis and persistent HPA dysregulation should be associated with a greater likelihood of relapse or chronicity. The combined dexamethasone/corticotropin-releasing hormone test was administered twice to inpatients with major depression (N = 40), once after initiation of treatment and once after remission, shortly before discharge. Patients with a high cortisol response on both occasions or with a substantially increased cortisol response at discharge were at much higher risk for relapse within the next 6 months than those with low cortisol responses. An easy-to-administer neuroendocrine test allows the prediction of medium-term outcome in patients with remitted depression.

Additive effects, but no synergistic interaction of stressful life-events and genetic loading in affective disorders.

Life-event research as well as neurobiological findings point to the relevance of adverse stress for the pathogenesis of affective disorders. The well established genetic root might be related to the sensitivity to stress. In concordance, recent studies showed a synergistic interaction between genetic loading and life-events concerning the precipitation of depression, i.e. there might exist a genetic sensitization to the adverse effects of stressors. The present investigation, using information extracted from 877 case records, did not reveal a synergistic interaction concerning the age at onset and the mean frequency and duration of episodes.

Neuroendocrine Mechanisms and the Precipitation of Depression by Life Events

It is now generally accepted that stressful life events and chronic difficulties can trigger the onset of depression in predisposed individuals. However, although much is known of the neurobiology of stress, few attempts have been made to provide a biological explanation for the mechanisms whereby life events might trigger depression. Enough is now known of the central control of hypothalamic pituitary adrenal (HPA) function and its response to stress to permit an examination of its role in the neurobiology of the triggering of depression by stress. This evidence is reviewed, and the proposal explored that stress triggers depression by a genomic action of corticosteroids.

Cognitive and life stress predictors of relapse in remitted unipolar depressed patients: test of the congruency hypothesis.

Remitted depressed subjects (N = 59) were followed longitudinally to determine whether dependent or self-critical persons are more vulnerable to relapse after exposure to life events that have a bearing on interpersonal or achievement concerns. Regression analyses indicated that congruency effects, as measured by the occurrence of achievement-related adversity in the lives of self-critical subjects, accounted for a significant increment in relapse variance over each variable entered singly. When data from the 2 months just before relapse were analyzed, some evidence of congruency effects in dependent subjects experiencing interpersonal-related adversity was obtained. These findings highlight the dimensional qualities of life even impact and call for greater differentiation in modeling the activation of a diathesis and precipitation of depression after life stress.

Factors involved in the regulation of adrenocorticotropic hormone/beta-lipotropic hormone.

Factors involved in the regulation of adrenocorticotropic hormone/beta-lipotropic hormone.