Active clinical trials for "Depressive Disorder, Major"

Major depression is accompanied by cognitive changes as well as alterations in multiple physical functions. The inflammatory system is altered generally toward a pro-inflammatory state. Antidepressants are associated with a decrease in this proinflammatory state. This study aims to generate pilot data concerning a possible link between cognition, inflammation and response to treatment. The cognitive function of subjects with major depression will be tested before and after treatment with duloxetine. Inflammatory markers will be measured at both time points.

Objective There is growing evidence showing a relation between depression, metabolic syndrome, diabetes, cardiovascular disease (1), serum lipid profile (2,3) and body weight (4), as well as the effects of some of the antidepressant medications on these various conditions and profiles. The aim of the study is to examine the influence of antidepressant medications on the metabolic profiles (5) of patients suffering from Major Depressive Disorder (MDD). Group of patients: 30 Patients aged 18-65, who were diagnosed with MDD according to the DSM-IV criteria. Research Design and Methods: Research duration will be 8 weeks. Patients meeting the inclusion criteria will be recruited after being diagnosed with MDD and having undertaken the HDRS. A follow-up HDRS will be taken at weeks 4 and 8. The psychiatric evaluation will be held by a resident in psychiatry. The following metabolic parameters will be examined at base-line and at the end of the 8 weeks: Weight, height, waist circumference, body mass index (BMI: (Weight in Kg/(Height in meters)2), sitting blood pressure (after 3 minutes of sitting). Serum lipid profile (performed in Ziv hospital's chemistry lab): Low density lipoprotein cholesterol, High density Lipoprotein cholesterol, Triglycerides, Total cholesterol, Apolipoprotein level (Apo AI, Apo B, Apo E, Apo AII). Fasting glucose and insulin blood levels, in order to evaluate insulin-release and resistance, according to the following formulas: Insulin Resistance: HOMA IR=Fasting glucose (mg/dL)x Fasting insulin (mmol/L)/405 Insulin Release: HOMA-β={360xfasting insulin (mmol/L)}/{glucose(mg/dL)-63} Serum oxidative stress parameters according to the F2-Isoprostane kit will be measured. Malonylaialdehyde (MDA) content in serum will be analyzed by the thiobarbituric acid reactive substances assay, which measures malondialdehyde equivalent (13). Conjugated dienes will be measured at 234nm (14, 15).

Selective serotonin reuptake inhibitors (SSRIs) raise serotonin (5-HT) in the synaptic cleft and are the current first line of pharmacological antidepressive treatment. Yet, there is a missing link between this first molecular step in their mechanism of action and observed clinical improvement. We have determined to establish a framework combining genuine molecular and functional imaging, i.e. hybrid pharmaco-PET/MR imaging, of the human serotonergic system in order to predict antidepressant treatment response. Objectives: To predict antidepressant treatment response from data obtained using hybrid PET/MR with acute pharmacological challenge. To discriminate healthy from depressed subjects using this paradigm. To establish models connecting regional changes in occupancy of serotonin transporters (5-HTT) following citalopram infusion, with changes in brain activation and connectivity of major resting-state hub networks. Design: Randomized, double-blind, placebo-controlled, cross-over mono-center study. Materials and methods: 40 major depressed (MDD) and 40 healthy subjects will undergo 2 PET/MR scans on a 3T SIEMENS mMR Biograph scanner: 1. challenge with citalopram 8mg 2. placebo (saline). After structural imaging, functional MRI will be continuously acquired. [11C]DASB will be applied using a bolus + constant infusion paradigm to probe 5-HTT binding potentials and monitor 5-HTT occupancy with drug challenge, applied after 70min, in a single session. Scanning will be terminated 80min after challenge. MDD patients will receive subsequent escitalopram treatment with repeated evaluation of response for 3 months.

Major depression disorder (MDD) has high estimated lifetime prevalence rates of 16.6%. Currently, the diagnosis for the MDD mainly depends on patients' reports of symptoms, observed behaviors and disease course. Establishment of clinically useful biomarkers for the MDD diagnosis would enhance patient management and treatment effect, and lead to the therapies adjusted to the individual. However, no such biomarkers have been established up to now. Therefore, the development of objective and feasible biomarkers is of special significance and a great challenge for accurate and early diagnosis and treatment of depression, in order to overcome the limitations of relying on clinical interviews alone.The ability to correctly recognize emotional states from faces is instrumental for interpersonal engagement and social functioning. Impairments processing of facial emotional expressions and biased facial emotion detection are frequently found in the MDD patients. To date, the studies on neural mechanism of the facial emotion recognition of the MDD patients were mainly based on the functional magnetic resonance imaging (fMRI). Functional near-infrared spectroscopy (fNIRS) has not been applied for the facial emotion recognition for the depression patients up to now. To bridge the important gap in the literature, we used the fNIRS methodology to investigate the neural mechanisms of facial emotion recognition for the patients with depression. We hypothesize the physiological feature of the hemodynamic responses in prefrontal cortex measured by fNIRS under the task of face emotion recognition, including the difference of the median, the Mayer wave power, the mean cross wavelet coefficient, and the mean wavelet coherence coefficient, combined with the behavior measurement (behavior accuracy and response time), could provide a reliable and feasible diagnosis approach to differentiate patients with the MDD from healthy control (HC) subjects with acceptable sensitivity and specificity.

Given the importance of cognitive function on depressed patients' treatment outcome and return to premorbid functioning, the effect of antidepressant drugs on cognition has become of primary concern. The aim of the present study is to assess the clinical outcome of switching from a selective serotonin reuptake inhibitor (SSRI) to desvenlafaxine on cognitive function in a Spanish sample of adults with moderate to severe major depressive disorder (MDD). This open-label clinical study will include a total of 36 MDD outpatients receiving treatment with desvenlafaxine according to treating psychiatrist clinical judgment. The primary efficacy endpoint will be changes from baseline to week 12 in cognitive function measured by a composite z-score comprising the Digit Symbol Substitution Test (DSST) and Rey Auditory Verbal Learning Test (RAVLT) scores. The secondary efficacy endpoints will involve depression severity, additional measures of subjective and objective cognitive function (including cold and hot cognitive function tasks), and functional status. A matched sample of 36 healthy controls will be assessed in order to obtain reference data for all cognitive function measurements. Patients with MDD and healthy controls will be compared regarding cognitive function both at baseline and after 12 weeks.

The study is designed as an open label, one arm study. Up to 30 eligible patients will be enrolled, for whom the Predictix Antidepressant Software tool will be used when prescribed with a medication for their Major Depressive Disorder, by their treating physician. Visits will include the completion of several questionnaires designed to answer the study objectives, either as self-reported by the subjects and/ or by the clinician.

The purpose of this randomized, placebo-controlled study is to investigate pharmacodynamic differences between racemic ketamine and esketamine using functional fluorodeoxyglucose ([18F]FDG) positron emission tomography/magnetic resonance imaging (PET/MR)

The objective of this transversal study is to determine if there is a difference in the volume of the hippocampus with the degree of anxiety.

Analysis of recent studies show that researchers find it hard to distinguish between Late Onset Depression, a first diagnosed major depressive episode which occurs at old age, and Early Onset Depression, a depressive episode at old age with a history of previous episodes. Since current data, about the phenomenology and etiology of Late Onset Depression, lake conicity it is unclear whether this phenomena should be considered as a distinct subtype of depression. Nevertheless, the wide spread assumption is that Late Onset Depression has a stronger correlation with brain damage and environmental risk factors such as the common losses at old age and weaker correlation with family history and genetics when compared to Early Onset. Although many researchers consider brain damage to have the main contribution to the emerge of Late Onset Depression, the fact that depression has a negative effect on one's health supports the claim that it might be the result and not the rick factor. Since Late Onset Depression correlates with the common losses at old age, the investigators propose that an existential approach that deals with one's meaning, freedom, responsibly and death, might be more appropriate. Thus, the investigators ask how do older adults experience depression which they face for the first time in old age? Current study will seek to understand older adults' experience of Late Onset depression through existential paradigm by using a semi constructed interview.

All subjects completing the randomized treatment period in Protocol NS2014-1 will discontinue study drug and be asked to provide consent to be followed in this 6-month study, at their final safety visit. The study will consist of an enrollment visit, followed by bi-monthly in-clinic visits with monthly telephone visits between in-clinic visits.