Active clinical trials for "Depressive Disorder, Major"

The purpose of this study is to determine if having an alcohol use disorder affects recovery from depression, and also whether recovery from depression in patients who have alcohol use disorders is also accompanied by improvement in the alcohol use disorder.

To facilitate the development of a personalized approach to the treatment of patients with major depression, this study is designed to elaborate the clinical and neurobiological phenotype of depressed patients with increased inflammation. The data obtained in this proposal will allow the investigators to test the hypothesis that depression and inflammation interact to elaborate a relatively discreet phenotype that warrants an individualized approach to diagnosis and treatment of patients with depression. Moreover, the identification of specific environmental risk factors for inflammation will foster the elaboration of preventative strategies for patients at risk.

The primary objective of this study is to provide duloxetine to investigators for the treatment of patients who have previously participated in neuroscience duloxetine clinical trials and for whom effective alternative therapy is not available.

Anxiety in children of parents with major depressive disorder (MDD) poses a particularly high risk for later-life MDD. In adults, MDD involves dysfunction in prefrontal brain regions that regulate attention to emotional stimuli. These abnormalities: i) have been found primarily in adults with specific familial forms of MDD; ii) persist after recovery from MDD, and iii) relate to anxiety. These findings raise the possibility that risk for MDD is tied to dysfunction in prefrontal regions involved in regulation of emotion, which possibly manifests as early-life anxiety. If this possibility were confirmed in never-depressed adolescents at high risk for MDD, the findings would provide key insights into the developmental neurobiology of MDD. The goal of this protocol is to study the neural substrate of risk for MDD in young people. This protocol tests the hypothesis that adolescents at high risk for MDD by virtue of childhood anxiety and parental history of MDD exhibit dysfunction in prefrontal cortex and amygdala, regions involved in emotion regulation. This goal will be accomplished through fMRI studies of emotion regulation in high and low-risk adolescents. For this research, at-risk adolescents will be recruited from participants in an NIMH-funded extramural study at New York University (NYU) examining the biology of risk for anxiety and depressive disorders. Over a three-year period, 45 high-risk probands and 60 low-risk comparisons will be studied, including 20 comparisons from the NYU sample and 40 from the Washington DC metropolitan area. In the present protocol, to be conducted at NIH, subjects will undergo volumetric MRI scans to assess structural abnormalities in the prefrontal cortex and medial temporal lobe. They will complete a series of four out-of-scanner cognitive tasks and two fMRI-based cognitive tasks that measure modulation of attention to emotional stimuli. The fMRI tasks are hypothesized to differentially engage the prefrontal cortex and amygdala in low vs. high risk subjects. These tasks will be used to test the hypothesis that at-risk individuals exhibit enhanced amygdala and reduced prefrontal activation on the fMRI emotion/attention tasks.

The purpose of the study is to describe the pharmacological and non-pharmacological treatment utilization pathways in Italian routine clinical practice of participants with Major Depressive Disorder (MDD) and active suicidal ideation with intent.

Patients who suffer from MDD recieved ketamnie (2014-15) in open study will be addressed and there depression mood will be evaluated using the rating scale that were used in the original research. In addition time of relapse and questions about their medications and drug use will be performed.

Major Depressive Disorder (MDD) is the leading cause of disability worldwide. Depression and anxiety disorders are among the most prevalent of all mental disorders, with an estimated annual prevalence of 9.7% and 18.1% respectively. It has been known for the last 100 years that depression and anxiety both likely affect vocal acoustic properties. In 1921, Emil Kraepelin, characterized depressed patient's voices as having a lower pitch, lower volume, lower rate of speech, more monotony of prosody as well as more hesitations, stuttering, and whispering. Mechanistically, it is possible that the neural circuitry involved in the pathophysiology of mood and anxiety disorders impinge upon the neural circuit involved in speech production, affecting qualities that include rate, prosody, speech latency and other paralinguistic features. Thus, acoustic features of speech may be one of the more readily accessible biomarkers for these conditions. Given this understanding, the investigators sought to develop a passive vocal biomarker instrument for depression and anxiety screening that could markedly expand access as well as standardize the quality of screening in primary care settings.

The primary aim of this project is to test if OCOsense glasses can function as a digital phenotyping tool derived from behavioural and physiological signals related to facial expression and motion recorded using the glasses.

This is a non-randomized, single-case design of pharmacogenetic implementation in a mental health patient population of subjects taking antipsychotics and/or antidepressants.

The purpose of this study is to validate a set of signatures, based on a panel of proteomic markers, that discriminate BDI, BDII, and MDD in people seeking treatment for a depressive episode.