View clinical trials related to Depressive Disorder, Major.
Filter by:The primary study intent is to examine biological mechanisms associated with acute and chronic treatment responses in major depressive disorder (MDD). It is hypothesized that treatment responsiveness, representing endogenous opioid system function, will be associated with acute improvements in mood state over a 10-week treatment trial in MDD. Potential (bio) markers of treatment effects will be tested against psychophysical responses to placebo and active treatments.
The purpose of this study was to evaluate the feasibility and compliance with a novel method for assessing mood and cognition in participants with major depressive disorder (MDD).
Background: Most medications that treat depression take weeks or months to work. Researchers want to develop fast-acting treatments. One dose of ketamine has a rapid antidepressant effect. For most people, this lasts a week or less. Repeated doses of ketamine may help maintain this effect. Objective: Main Study: To study the effects of ketamine in treating depression. Ketamine Metabolites Substudy: To study how ketamine effects brain chemistry. To study how ketamine effects the brain. This is done by looking at metabolites, which are created when a drug is broken down. Eligibility: Main Study: People ages 18-65 with major depressive disorder and healthy volunteers Ketamine Metabolites Substudy: Healthy volunteers ages 18-65 Design: Main Study: Participants will be screened in another study, with: - Medical and psychiatric history - Psychiatric and physical exam - Blood, urine, and heart tests Participants will be inpatients at NIH for 4 phases totaling 14-20 weeks. Phase I (2-7 weeks): - Gradually stop current medications - MRI: Participants lie and perform tasks in a machine that takes pictures of the body. - Mood and thinking tests - Blood and urine tests - Sleep test: Monitors on the skin record brain waves, breathing, heart rate, and movement during sleep. - Transcranial magnetic stimulation: A coil on the scalp gives an electrical current that affects brain activity. - Stress tests: Electrodes on the skin measure reactions to loud noises or electric shocks. Phase I tests are repeated in Phases II and III and in the final visit. Phase II (4-5 weeks): - 4 weekly IV infusions of ketamine or a placebo during an MRI or MEG. For the MEG, a cone over the head records brain activity. Phase III (optional): - 8 infusions of ketamine over 4 weeks Phase IV (optional): - Symptoms monitoring for 4 weeks - Participants will have a final visit. They will be offered standard treatment at NIH for up to 2 months. Ketamine Metabolites Substudy: Participants will be screened in another study, with: - Medical and psychiatric history - Psychiatric and physical exam - Blood, urine, and heart tests Participants will be inpatients at NIH for 4 days. Study Procedures: Mood and thinking tests Blood and urine tests 1 infusion of ketamine Spinal tap and spinal catheter: Used to get samples of cerebrospinal fluid (CSF). This is a fluid that moves around and within the brain and spinal cord. Studying CSF will help us learn how ketamine effects brain chemistry
Background: The gut microbiome is emerging as an important factor in regulating mental health yet it remains unclear what the target should be for psychiatric treatment. Investigators aim at elucidating the complement of the gut microbiome community for individuals with Major Depressive disorder (MDD) and Bipolar disorder (BD) relative to controls, and test for relationships with symptoms. Methods: Investigators prospect to recruit subjects including patients and controls amount to 240. All subjects will be collected for blood and stool samples,assessed by clinical scales. Finally, analyzing the correlation among the metabolon in blood, microbiota in stool and clinical scales to obtain the possible interaction between diseases and gut microbiota.
Testing an mHealth mobile interventionist texting program on illness management.
The steroid hormone cortisol is released in response to stress and acts in the central nervous system upon glucocorticoid (GR) and mineralocorticoid receptors (MR). GR are widely distributed across the brain while MR are predominantly expressed in the hippocampus and prefrontal cortex - two brain areas closely related to memory and executive function. Stimulation of MR leads to an increase of glutamate that act on glutamatergic NMDA receptors in the hippocampus and prefrontal cortex. In previous studies, the investigators have shown that fludrocortisone, a mineralocorticoid receptor (MR) agonist, improves memory and executive function in depressed patients and healthy controls. However, depressed patients not only exhibit cognitive deficits in traditional neuropsychological domains such as memory or executive function. In addition, there are depression-specific alterations such as cognitive bias and deficits in social cognition, two clinically highly relevant areas. Therefore, the specific aims of this renewal proposal are two-fold: - To examine whether beneficial effects of fludrocortisone in depressed patients can be extended to depression-specific cognitive bias and to social cognition - To determine whether beneficial effects of fludrocortisone depend on NMDA-receptor function and whether these beneficial effects can be enhanced by NMDA receptor stimulation. The investigators hypothesize that fludrocortisone will improve cognitive bias and social cognition in depressed patients and that its beneficial effects depend on the NMDA receptor. Therefore, the investigators further hypothesize that the effects of fludrocortisone can be enhanced by co-administration of the partial NMDA receptor agonist D-cycloserine. The study not only advances current knowledge by further examining the mechanism of action by which MR stimulation exerts beneficial effects on cognition but extends these effects to depression-specific cognitive bias and alterations in social cognition. Furthermore, a potential interaction between MR and NMDA receptors is highly clinically relevant given the promising results with NMDA receptor antagonists in the treatment of major depression.
Major depression is a frequent psychiatric disorder with an estimated lifetime prevalence of 16-17% in the general population. Although its pathophysiology is not completely understood, a large body of literature pleads for a causative role of disturbances in reward processes, referring to: i) the hedonic sensation (i.e. "liking") defined by the pleasure felt after exposure to appetitive stimuli, and ii) the motivation (i.e. "wanting") represented by the ability to initiate and maintain behavioral responses oriented toward appetitive stimuli. the investigators have therefore developed and tested a new experimental computer-based and easy-to-use test intended to provide an objective and quantitative measurement of both hedonic and motivational states in humans. According to the task, the subjects are asked to view and to compare two stimuli, an appetitive one (food pictures) and its devalued counterpart (food pictures in greyscale), at each trial, assessing either the size (task A) or the duration of presentation (task B). From these considerations, the present project aims at using our novel tool to: i) assess the hedonic and motivational state in subjects with major depression, ii) compare their responses with healthy volunteers. The present project should demonstrate that the behavioral tests validated in our laboratory are relevant experimental tools for the diagnostic/clinical assessment and for the phenotypic characterization of depressed patients. The application of the test in the therapeutic context could add further information about the efficacy and relevance of the chosen therapy.
Medically healthy Veterans ages 21-75 that have been diagnosed with Depression will get up to 6 treatments of Ketamine infusions, weekly. After treatment is completed, follow up will occur at 1 month, 3 months, and 6 months after completion of infusions to evaluate the longer term effects of ketamine.
The purpose of this study is to evaluate the sensitivity of the THINC-it tool, in measuring change in cognitive deficits in individuals with MDD after receiving vortioxetine.
Demonstrate the acute effects of ketamine on endogenous µ-opioid neurotransmission in humans.