View clinical trials related to Depressive Disorder, Major.
Filter by:The study will compare two groups of patients: a control group of patients treated per the Standard of Care when prescribed with a medication for their Major depression disorder, versus a group of patients that used the Predictix Antidepressant tool when prescribed with a medication for their Major depression disorder by their treating physician. Success will be measured by the number (proportion) of responders per group.
This study aims to openly test the long-term safety, tolerability and effectiveness of repeated administration of IM/SC ketamine for treatment resistant MDD.
Background: MDD is a common mental disorder with significant morbidities and mortalities. Recent local data suggested that depressive disorders have a prevalence of over 12% in females and nearly 7 % in males in Hong Kong general adult population. Other than insomnia, patients with MDD often complained another sleep symptom - hypersomnia (defined as daytime sleepiness or excessive sleep). Interestingly, when compared to insomnia, there is much far less research on the role of hypersomnia in MDD. However, there are available data suggested that hypersomnia is associated with greater treatment-resistance, more recurrence, and increased suicidality, suggesting a need to investigate this problem in MDD patients. Objective: To investigate the prevalence and determine characteristics of hypersomnia amongst major depressive disorder. Design: 2-phase study design Setting: A case-control study Participants: Patients with a history of Major Depressive Disorder from out-patient clinics in New Territories East Cluster. Main outcome measures: Daytime sleepiness measured by MSLT, actigraphy and self-reported questionnaire (ESS), sleep duration as measured by sleep diary and actigraphy.
Neurons are specialized types of cells that are responsible for carrying out the functions of the brain. Neurons communicate with electrical signals. In diseases such as major depression this electrical communication can go awry. One way to change brain function is using electrical stimulation to help alter the communication between groups of neurons in the brain. The purpose of this study is to test a personalized approach to brain stimulation as an intervention for depression. The study researchers will use a surgically implanted device to measure each individual's brain activity related to his/her depression. The researchers will then use small electrical impulses to alter that brain activity and measure whether these changes help reduce depression symptoms. This study is intended for patients with major depression whose symptoms have not been adequately treated with currently available therapies. The device used in this study is called the NeuroPace Responsive Neurostimulation (RNS) System. It is currently FDA approved to treat patients with epilepsy. The study will test whether personalized responsive neurostimulation can safely and effectively treat depression.
Repetitive transcranial magnetic stimulation (rTMS) has become a safe and efficacious treatment for patients with treatment-resistant depression. In several studies investigating the antidepressant efficacy of rTMS, it has been shown that in low treatment-resistant patients rTMS is more efficacious than in patients where several treatment attempts have failed. Albeit this finding, most studies to date primarily recruited patients with relatively high degrees of treatment-resistance and there is a lack of trials investigating rTMS as a first-line treatment. Therefore, this trials aims to compare the antidepressant efficacy of 4 weeks open-label theta-burst TMS in non-treatment-resistant patients with a comparable group of treatment-resistant MDD patients.
Background: Most drugs that treat mood disorders take a long time to work. Ketamine works within hours. A dose can last for a week or more. Certain receptors in the brain might help ketamine work. A drug that blocks these receptors might affect how it works. Objective: To see if the antidepressant response of ketamine is linked to AMPA receptors. Eligibility: Adults ages 18-70 with major depression disorder without psychotic features Design: Participants will be screened under protocol 01-M-0254. They will have blood tests and a physical exam. Participants will stay at the NIH Clinical Center for 5 weeks. Phase 1 lasts 4 weeks. For 2 weeks, participants will taper off their psychiatric medicine. Then they will have the following tests: - Blood draws - Psychological tests - MRI: Participants will lie in a machine that takes pictures of their brain. - MEG: Participants will lie down and do tasks. A cone lowered on their head will record brain activity. - Optional sleep tests: Electrodes on the scalp and body and belts around the body will monitor participants while they sleep. - Optional TMS: Participants will do tasks while a wire coil is held on their scalp. An electrical current will pass through the coil that affects brain activity. For phase 2, on day 0 participants will take the study drug or a placebo orally. While having a MEG, they will get ketamine infused into a vein in one arm while blood is drawn from a vein in the other arm. On day 1, participants will again take the study drug or a placebo orally. On days 3-7, they will repeat many of the phase 1 tests. Days 8 and 9 are optional and include an open label ketamine treatment and many of the phase 1 tests.
The purpose of this study is to identify pharmacogenetic profiles associated with selective serotonin reuptake inhibitors (SSRI)-induced behavioral disinhibition in children with Major depressive disorder (MDD), anxiety disorders and/or obsessive-compulsive disorder (OCD) that could be used clinically to reduce the incidence of this adverse event and improve health outcomes.
This study aims to investigate changes in functional connectivity over a four week treatment course with intermittent theta burst stimulation (iTBS) in patients with major depressive disorder (MDD). To this end, seven weekly resting-state fMRI (rs-fMRI) scans at 7 tesla (7T) will precede, accompany and follow the iTBS treatment course. By obtaining several samples of the modulatory effects of iTBS on functional connectivity networks and simultaneous measurements of the depressive symptoms it will be possible to assess the time course of changes in connectivity across different networks, and to assess the overall relationship between the network modulation and the antidepressant effects of the treatment over time.
The overarching aim of the study is to determine the role of insulin signaling on the neurobiological substrates subserving anhedonia within individuals with mood disorders (i.e., Bipolar Disorder (BD) and Major Depressive Disorder (MDD)). Specific aims include: 1. Molecular: Assessment of components of the insulin cascade, as well as of anhedonia and reward-related processes, using a proteomics and gene expression approach; 2. Physiology: Measurement of peripheral sensitivity to insulin and metabolic correlates, including body mass index and dyslipidemia; 3. Neural Circuits: Evaluation of the insulin sensitivity of prefrontal (e.g. prefrontal cortex) and striatal (e.g. nucleus accumbens, ventral tegmental area) networks in the resting-state and during an effort-based decision making test, using acutely administered intranasal insulin and functional magnetic resonance imaging (fMRI); 4. Behavioral: Measurement of willingness to make effort for rewards, as well as of other components of reward response and anhedonia, using validated behavioral tasks and clinical scales (e.g. Snaith-Hamilton Pleasure Scale - SHPS). This initiative represents a proof-of-concept study that insulin is important to anhedonia, neurocognitive functioning, and behavioural deficits in MDD, representing a novel and safe therapeutic avenue.
Depressive disorder is known as being accompanied with the activation of immune system which could lead to a series of changes including the neuron apoptosis, synapses transmission inhibition and emotional symptoms. The activation of protein kinase C (PKC) can reverse the immune/inflammatory process and restore the neuroplasticity and neurotransmitters transmission. Based on our finding that patients with major depressive disorder (MDD) showed a significantly lower gene expression of PRKCB1, while the PKC activation mediated by PRKCB1, we hypothesize that PRKCB1 contribute to the development of MDD and treatment response by its specific expression in brain, regulating ERBB, Chemokine signaling pathways and PKC activation during the neuroinflammatory process. In the present study, we aim to evaluate and verify the regulation effect of PRKCB1 on the neuroimmune and inflammatory mechanism in depressive disorder by a serious of studies focus on PRKCB1 gene expression modulating process and different downstream biomarkers which associated with PRKCB1 effect, combined with the specified treatment (plus omega-3 poly unsaturated fat acids). This study may provide scientific evidences for using neuroinflammatory biomarkers to diagnose MDD, as well as personalized treatment.