View clinical trials related to Major Depression.
Filter by:This study aims at evaluating the effect of electroconvulsive therapy in treatment-resistant depressed patients on the major serotonin degrading enzyme in the human brain using neuroimaging methods, the monoamine oxidase A. Electroconvulsive therapy is an effective treatment option in severe cases of depression. However, the mechanisms underlying its effect remain uncertain, though variations within the serotonergic neurotransmitter system seem to be crucially involved.
The purpose of this study is to determine wether peer support is effective for the treatment of people with severe mental illness.
Background: Mindfulness has its origins in an Eastern Buddhist tradition that is over 2500 years old and can be defined as a specific form of attention that is non-judgemental, purposeful, and focused on the present moment. It has been well established in cognitive behavior therapy in the last decades, while it has been investigated in manualized group settings. Consequently, the demand to investigate mindfulness under effectiveness conditions in trainee therapists has been highlighted. Methods/Design: To fill in this research gap, the investigators designed the PrOMET-Study. In this study, the investigators will analyze the effects of brief, audio-tape presented, in-session mindfulness interventions conducted by both trainee therapists and their patients at the beginning of individual therapy sessions in a randomized, controlled longitudinal design under effectiveness conditions in a total of 30 trainee therapists and 150 patients in a large outpatient training center. The investigators hypothesize the mindfulness intervention will have positive effects on therapeutic processes and outcome in contrast to a progressive muscle relaxation and a treatment as usual group. The investigators will conduct multilevel modeling to address the nested data structure. Discussion: The study results could provide important practical implications, as they could inform ideas on how to improve clinical training of psychotherapists that could be implemented very, as there is no need for complex infrastructures or additional time concerning these brief, in-session mindfulness interventions that are directly implemented in treatment sessions.
The investigators propose to examine both resting state activity and functional activity during rumination and during self-processing to study the relationship between neural correlates of rumination/self-focus and self-processing in major depression and bipolar disorder.
The proposed study will evaluate the response and remission rates for major depressive disorder (MDD) in end-stage renal disease (ESRD) patients undergoing maintenance hemodialysis (HD) treated with bupropion or fluoxetine for 12 weeks. In addition, the study will document the relative tolerability and safety, and longitudinally contrast the effects of bupropion and fluoxetine on measures of cognitive function, fatigue, inflammation, and tryptophan (TRP) and TRP catabolites in blood. It is hypothesized that both drugs will significantly reduce MDD symptoms from baseline, and be tolerable and safe, but bupropion will be associated with greater reduction in pro-inflammatory cytokines, cognitive impairment, and fatigue compared with fluoxetine. The Specific Aims of this study are: Aim 1: Determine the efficacy of bupropion and fluoxetine in treatment of MDD in ESRD/HD patients. Aim 2: Determine whether longitudinal change in MDD symptoms, cognitive dysfunction, and fatigue differ between bupropion and fluoxetine. Aim 3: Determine whether longitudinal change in MDD symptoms, cognitive dysfunction, and fatigue correlate with change in inflammation, measures of TRP availability to brain, or neurotoxic TRP metabolites. Hypotheses: 1. Bupropion and fluoxetine will both show efficacy in treating MDD; 2. Bupropion will lead to greater improvement in cognitive dysfunction and fatigue than fluoxetine; and 3. Change in cognition and fatigue over time will correlate with change in c-reactive protein (CRP) and quinolinic acid and change in overall depression score will correlate with measures of TRP availability.
The study evaluates the ABCB1-genotype dependent efficacy of a quick dose-escalation strategy within 28 days of treatment with approved antidepressants that are known substrates of the P-glycoprotein, an efflux pump of the blood-brain barrier expressed by the ABCB1 gene. Moreover, the study evaluates ABCB1-genotype dependent side-effects of approved antidepressants that are known substrates of the P-glycoprotein, an efflux pump of the blood-brain barrier expressed by the ABCB1 gene.
The purpose of this study is to evaluate clinical efficacy (affective and cognitive) in patients with moderate depression between TMS over the left Dorsolateral Prefrontal Cortex (DLPFC) with simulated TMS, as well as clinical response when 5 sessions / week are applied vs. 2 sessions / week. All patients will receive 15 TMS sessions as initial treatment (active or sham) and respondents will participate in an TMS follow-up on the left DLPFC for three months.
To examine whether the medial prefrontal cortex displays an increased activity during self-referential processing among remitted depressed patients compared to healthy controls
Despite the public health importance of clinical depression, more than 50% of depressed adults receive inadequate or no treatment, with even higher rates of under-treatment in men and minorities. Family members and/or friends often assist older adults in their health care and may help overcome barriers to formal care, yet there is a lack of primary care-based interventions that mobilize family members and friends to improve depression treatment. In partnership with a community-based clinic, this research will address this scientific gap by developing and then testing the feasibility and acceptability of a family-based intervention that can be delivered pragmatically in a primary care setting serving large numbers of older minorities.
A single subanesthetic dose infusion of the N-methyl-D-aspartate (NMDA) receptor antagonist ketamine has rapid and robust antidepressant effects in patients with treatment-refractory major depressive disorder (TRD). A family history of an alcohol use disorder (Family History Positive, FHP) is one of the strongest identified predictors of an improved antidepressant response to ketamine. Like ketamine, alcohol is a functional NMDA receptor antagonist. FHP is associated with differential response to ketamine, e.g. blunted psychotomimetic side effects. One of the primary mechanistic hypotheses for ketamine's antidepressant action is the acute intrasynaptic release of glutamate from major output neurons, e.g. cortical pyramidal cells. Preliminary clinical studies have demonstrated this acute glutamate "surge" in response to subanesthetic dose ketamine. Based on these findings, the investigators hypothesize that ketamine's enhanced antidepressant efficacy in FHP TRD subjects is, at least in part, attributable to increased glutamate release relative to TRD subjects without a family history of alcohol use disorder (Family History Negative, FHN). To test this hypothesis, the investigators have designed a now two-site, open-label study of 18-55-year-old medically and neurologically healthy, currently moderately-to-severely depressed TRD patients. In total, the investigators plan to recruit 25 FHP and 25 FHN TRD subjects. All subjects must not have a lifetime substance use disorder (except nicotine or caffeine) and no lifetime history of an alcohol use disorder. The experimental portion consists of two phases. The preliminary first phase is a medication taper (if needed) and psychotropic medication-free period. The experimental second phase comprises one subanesthetic dose (0.5mg/kg x 40 minute) ketamine infusion. The ketamine infusion will occur during 7T-magnetic resonance imaging (MRI), both resting-state functional MRI (rs-fMRI) and magnetic resonance spectroscopy (MRS) to detect glutamate in the ventromedial prefrontal cortex/ventral anterior cingulate cortex (vmPFC/vACC). The primary outcome measure is group mean change in Montgomery-Åsberg Depression Rating Scale (MADRS) score from pre-ketamine infusion (baseline) to one-week post-infusion, where the investigators observed ketamine's greatest antidepressant effect in FHP TRD. Additional outcome measures are vmPFC/vACC glutamate change in response to ketamine based on family history status. In summary, this study will provide key mechanistic information on ketamine's improved antidepressant efficacy in a biologically-enriched subgroup. This will contribute to the systematic development of more efficacious, personalized treatments for major depression in an effort to reduce its enormous public health burden.