Active clinical trials for "Depressive Disorder, Treatment-Resistant"

This study is a multicenter prospective, parallel design, two-arm, rater-blinded randomized controlled pilot trial. Participants will be randomly assigned to one of two treatment conditions. In the first condition, treatment consists of rTMS sessions combined with Text4Support. The second condition is made up of the treatment as usual (rTMS sessions alone). The recruitment process is scheduled to last 12 months. It will involve active treatment for six weeks and follow-up period observation periods of 1,3, and 6 months for participants in both arms of the study. Participants will be recruited from four different centers for this project. Two centers (the Addiction and Mental Health clinic and the Alberta day hospital) will be from the large, sociodemographic diverse city of Edmonton in Alberta Western Canada. The remaining two centers will be in Halifax and Annapolis Valley in Nova Scotia, Canada.

The primary objective of this multicenter, randomized, sham-controlled, double blind (patient and observer blinded) clinical trial is to assess the antidepressant effect of Deep Brain Stimulation (DBS) in patients with treatment resistant major depression using the Boston Scientific implantable Vercise™ GEVIA™ DBS system compared to sham.

Objectives of this study are to determine whether active VNS Therapy treatment is superior to a no stimulation control in producing a reduction in baseline depressive symptom severity, based on multiple depression scale assessment tools at 12 months from randomization.

This trial aims to assess the efficacy and tolerability of Magnetic Seizure Therapy (MST) and two different forms of electroconvulsive therapy (ECT) in sustaining response during and after a course of continuation treatment.

The goal of this clinical trial is to demonstrate the feasibility and safety of deep brain stimulation in treatment resistant depression. The main questions it aims to answer are: Is deep brain stimulation effective in treating treatment resistant depression? Does deep brain stimulation improve overall clinical well-being and functioning? Participants will be implanted with a deep brain stimulation device. They will then be monitored over a 5-year period by using multiple questionnaires to track their depression symptoms. The device will be turned off at certain time points, unbeknown to the participant, to show the efficacy of the device when it is turned on. The device will be ON for 8.5 months and OFF for 3.5 months during the first year. Researchers will compare questionnaire scores when the device is off versus on to see if the device is working in reducing depression.

This study will evaluate the efficacy and safety of NV-5138 in adults with TRD

The purpose of this research study is to find an alternative version of ECT that reduces the negative side effects (mainly memory loss) while still providing patients with relief from depressive symptoms. Previous forms of ECT may use Bilateral (electrodes on both sides of the head) or Right Unilateral (RUL) (electrodes on one side of the head). Our research focuses on adjusting the placement of electrodes on one side of the head in order to better stimulate the Prefrontal Cortex (PFC) of the brain. By more specifically targeting the PFC, it is predicted that participants will receive the same benefit as ECT but will have fewer negative side effects after the treatment, mainly less memory loss. All other aspects of the treatment will be similar to regular, clinical ECT, including anesthesia and recovery monitoring. To accomplish this stimulation, an adjusted MECTA Spectrum 5000Q device will be used. If successful, this research study will demonstrate a way to improve ECT procedures for all patients suffering from Major Depressive Disorder by minimizing side effects and maintaining or improving efficacy.

The aim of this randomized, double-blind, placebo-controlled, phase 2b clinical trial is to investigate the safety and efficacy of GH001 (containing mebufotenin [5-methoxy-N,N-dimethyltryptamine; 5-MeO-DMT]) in patients with treatment-resistant depression (TRD). The study is comprised of a 7-day double-blind (DB) part (Part 1) and a 6-month open-label extension (OLE) part (Part 2). Patients will be randomized to receive GH001 or placebo in a 1:1 ratio. The primary endpoint is the mean change in the Montgomery-Åsberg Depression Rating Scale (MADRS) from baseline to Day 7.

This study evaluates an accelerated schedule of theta-burst stimulation using a transcranial magnetic stimulation device for treatment-resistant depression. In a double-blind, randomized, sham-controlled fashion, half the participants will receive accelerated theta-burst stimulation while half will receive sham treatment.

Late-Life Depression (LLD), or depression in older adults, often presents with motivational deficits, deficits in performance in cognitive domains including processing speed and executive dysfunction, and mobility impairments. This triad of findings implicate dopaminergic dysfunction as a core pathophysiologic feature in depression, and may contribute to cognitive decline and motor disability. Normal aging results in brain-wide dopamine declines, decreased D1/D2 receptor density, and loss of dopamine transporters. Although brain changes associated with depression and aging converge on dopamine circuits, the specific disturbances in LLD and how responsive the system is to modulation remain unclear. In this study, investigators are testing integrative model that aging, in concert with pro-inflammatory shifts, decreases dopamine signaling. These signally changes affects behaviors supported by these circuits, in the context of age-associated cortical atrophy and ischemic microvascular changes, resulting in variable LLD phenotypes. Investigators propose a primary pathway where dopaminergic dysfunction in depressed elders contributes to slowed processing speed and mobility impairments that increase the effort cost associated with voluntary behavior. The central hypothesis of this study is that late-life depression is characterized by dysfunction in the dopamine system and, by enhancing dopamine functioning in the brain. By improving cognitive and motor slowing, administration of carbidopa/levodopa (L-DOPA) will improve depressive symptoms.