Active clinical trials for "Depression"

The objectives of this project are to determine if the bioavailability and release pattern of bupropion HCl products differ and if the genotype of the metabolic enzymes affects the saturation of intestinal enzymes with different dose strengths within one product line. Findings from this project will help the FDA Center for Drug Evaluation and Research's (CDER) Office of Generic Drugs improve policy development and review practice in the future for similar products, e.g. extended release oral drug products being metabolized in the gut wall and having multiple strengths. Aim 1: To compare the pharmacokinetics of bupropion and its metabolites in plasma in healthy individuals when they ingest different strengths of bupropion (75-300 mg) with variable release profiles (IR vs XL vs SR) in GI tract. Working hypothesis: Variation in release rate and mechanism of bupropion formulations in gastrointestinal (GI) tract will impact metabolism and saturation of bupropion in GI tract, which will generate different concentration of bupropion and its metabolites in plasma. Aim 2: To investigate pharmacogenomics of CYP 2B6 that influences metabolism, saturation, and pharmacokinetics of bupropion Working hypothesis: The gain of function of CYP2B6 variants (allele *4 and *22) in patients will increase the metabolism of bupropion in the GI tract and liver, reduce both local concentration and plasma concentration of bupropion, and thus cause non-bioequivalence when bupropion is released earlier in GI tract

The hypotheses were as follows: H1. Women at low-moderate risk for APD at T1 (baseline EPDS scores of 5-9) in the cognitive behavioral intervention (CBI) group will maintain low-moderate risk status and have significantly fewer APD symptoms at T2 and T3 than women at low-moderate risk for APD in the (TAU) control group (as measured by percent of participants with EPDS scores <9 at T2 and T3 and mean score changes). H2: Women at high risk for APD at T1 (baseline EPDS scores ≥10) in the CBI group will have a significantly greater reduction in APD symptoms at T2 and T3 than women at high risk for APD in the TAU control group (as measured by percent of participants with EPDS scores <10 at T2 and T3 and mean score changes).

The goal of the study is to examine the difference of the pharmacokinetics of metformin with and without a 3 weeks pretreatment of St John's Wort. Furthermore secondary objectives include changes in GLP-1, C-peptide, serum-insulin and plasma-glucose during an oral glucose tolerance test, changes in OCT1 mRNA in plasma and changes in leptin and lipid-profile following this possible interaction.

There is good evidence to suggest that the pathological version of sadness that people with Major Depression experience could be caused by the failure of the hormone cortisol to properly inhibit sadness-related brain activity in the subgenual cingulate cortex. This project investigates if the subgenual cingulate cortex has become insensitive to cortisol in patients with depression and tests for variants of the cortisol receptor genes that could predispose individuals to develop cortisol insensitivity.

The purpose of this study is to assess the effectiveness of a Relaxation Response Intervention for Depression offered to low income populations at Massachusetts General Hospital (MGH) - Chelsea, Revere and Charlestown health centers.

The purpose of the study is: To conduct a pilot SMART (Sequential, Multiple Assignment, Randomized) study with the long-term goal of developing a personalized treatment for child depression. To collect pilot data on ways to personalize treatment for child depression using cognitive behavioral therapy (CBT), caregiver-child treatment, or both.

The purpose of the study is to examine if blood flow in the brain before coronary artery bypass graft surgery has an effect on depression after surgery. The main hypothesis of the study states that pre-surgical blood flow in the brain will be an independent risk factor for depression after surgery after adjusting for other risk factors such as gender, pre-CABG depression, social support, medical comorbidity burden, socioeconomic status, and neuroticism.

Family caregivers are vulnerable to health problems because of the stress and demands of their role as a caregiver. With the growing incidence of heart failure (HF) and the anticipated growth in the aging population, the number of HF caregivers is expected to rise. This study will pilot test a cognitive behavioral intervention designed to reduce stress among HF caregivers, which will ultimately contribute to promoting health and quality of life among HF caregivers and their loved ones with HF.

Depression is a debilitating illness with a risk of developing a treatment resistant form. Currently, diagnosis is purely clinical with little features available to identify potentially adverse developments. Clinical features such as early onset age, prolonged episodes, anxiety, somatic symptoms and apathy are all arguments raising fears the onset of resistance to conventional treatments. According to neuroimaging knowledge about the pathophysiological mechanisms, involving front-limbic functional networks supporting the functions of emotional regulation and reward system, recent work has focused on the identification of neuroimaging biomarkers predicting therapeutic response. Among the regions of interest identified, the anterior cingulate cortex, amygdala, hippocampus, and regions participating in the Default Mode Network Training (Medial prefrontal cortex, posterior cingulate cortex, inferior parietal lobe) are most frequently areas associated with the prediction of therapeutic response. Limitations most reported in these studies are the heterogeneity of experimental paradigms (resting state, cognitive or emotional functional tasks), imaging (PET scan, MRI) the heterogeneity of clinical resistance criteria forms studied, different techniques (as that we consider remission (threshold score) or response (50% decrease from baseline score), and the sample size. Knowing that MRI into daily clinical practice in the SHU of Adult Psychiatry, as the balance sheet of the disease, monitoring its evolution, as in assumption rTMS (repetitive Transcranial Magnetic Stimulation) (pretreatment assessment and neuro), the identification of neuroimaging biomarkers in a population of patients with clinical criteria of Mood Depressive Episode, with an acquisition of identical and reproducible image daily routine methodology appears to be a reliable way to correct the heterogeneity of conventionally published studies on the topic. This study aim to identify, in routine care, predictive clinical and neuroimaging markers of poor outcome in major depressive disorder.

The investigators will (1) detect the associations between brain-derived neurotrophic factor (BDNF) DNA methylation, histone modification, depressive symptoms, suicidal behavior and antidepressant responses in major depressive disorder (MDD) patients, (2) check the correlation between blood BDNF protein and RNA and BDNF rs6265 gene, and (3) discuss the possible mechanisms of epigenetic regulation of BDNF in Taiwanese major depressive patients.