Active clinical trials for "Depressive Disorder"

Major depression disorder (MDD) is a frequent and disabling mental disorder with great risk of recurrence and chronicity. Interpersonal factors are among the strongest predictors of the course and duration of an episode of depression. More specifically, social rejection is one of the most environmental risk factors of MDD. Targeted rejection predicts hastened onset of major depression. On the other hand, healthy subject show prosocial behavior after social rejection to reconnect to new source of social interaction. In addition to the potential impact of social exclusion on MDD onset, depressed patients may be more prone to be rejected as they encounter interpersonal difficulties and may less be able to reconnect to the social group after rejection. Recent neuroimaging data show that brain processing of social exclusion activate brain regions that are central to the pathophysiology of MDD. Some of these regions are also known to be activated during physical pain and may contribute to the aversive dimension of the experienced rejection. Pro-inflammatory cytokines are involved in MDD physiopathology and can induce social withdrawal behavior. Inflammation can modulate social interactions in mammals. Moreover, after a social stress such as social rejection, blood cytokines increase. At a cognitive level, self-esteem can modulate the sensitivity to social rejection. The major objective of the trial is to study sensitivity to social signals in MDD patient compared to healthy subject. The investigators hypothesize in MDD patient : (1) decrease of rapid facial reactions (RFR) to dynamic emotional faces expressing joy, (2) increase of RFR to dynamic emotional faces expressing sadness, (3) decrease of prosocial reaction after experimental social rejection. Secondary objective is to identify psychological and biological mediators We hypothetize in MDD patient: (1)mediating effect of systemic inflammatory cytokines, an (2) mediating effect of state self esteem 30 MDD patients and 60 healthy subject will be included. They will encounter psychiatric and psychometric evaluation. Their facial EMG will be recorded to assess RFR to dynamic emotional faces created by photo morphing from KDEF emotional faces database, coupled to occulometric recording. Subjects will perform cyberball game as an experimental inclusion or exclusion task and the trustgame task as an implicit evaluation of their prosocial behavior. Questionnaires will assess explicit measurement of social rejection pain and desire of affiliation. Inflammatory markers will be measured in a blood sample before the cyberball task for every subjects and 6 hours later for 20 healthy volunteers. Dosage of IL-6, IL-10, TNFa, IP-10, MCP-1, MIP-1b, Rantes, sIL-6Ra, IL1ra, VEGF, Leptin, PECAM1, sTie2, sVEGFR1, sVEGFR2 will be performed by luminex technique and usCRP, srIL2 ans sCD14 by ELISA technique.

The overall goal of the proposed project is to investigate the neuronal pathways regulating the effects of social acceptance and rejection in healthy controls and patients with Major Depressive Disorder (MDD). Social acceptance and rejection are defined as the explicit declaration that an individual is liked or not liked. Social acceptance can boost one's self-esteem and mood, whereas rejection can lower them. The neurological relationship between social acceptance/rejection and depressive symptoms is not known. Using functional magnetic resonance imaging (fMRI), it is hypothesized that social feedback will activate a specific interconnected neuronal pathway involved in social separation and reward. Executive functioning and response to monetary reward will also be assessed during fMRI using two additional tasks (monetary incentive delay, parametric go no-go) to determine how these cognitive brain functions regulate responses to social feedback.

The long-term goal of this line of research is to determine if decreased vascular reactivity and frontal hypoperfusion is associated with poor response antidepressants. Such perfusion deficits could contribute to antidepressant nonresponse as they would hinder improvements in dorsal system metabolism seen with antidepressant treatment. The objective of the current proposal is to determine if decreased vascular reactivity and frontal hypoperfusion in depressed elders predicts and persists with antidepressant nonremission. The investigators will pursue the primary aim testing the hypothesis that decreased reactivity and hypoperfusion, specifically in the dorsolateral prefrontal cortex and dorsal anterior cingulate cortex, predict antidepressant nonremission. The investigators will enroll 40 depressed elders who will complete clinical, cognitive, and MRI assessments before and after a 12-week open-label antidepressant trial of sertraline.

The purpose of the funded study is to determine a) examine associations among OT levels, stress, trauma history, PPD, and lactation failure in the full 60-subject sample and assess whether there are differences between immigrant women and non-immigrant Latina women on these measures; b) quantify whether there is a correlation between ACTH, cortisol, and PPD and whether there are differences between immigrant and non-immigrant Latina women; and c) assess the feasibility of enrolling Latinas into a laboratory-based study that includes the collection of venous blood for measurement of oxytocin, ACTH, and cortisol. Sixty prenatal (34 to 37 weeks) Latinas (30 immigrants and 30 U.S.-born) who are between the ages of 18 and 45 will be enrolled. Women with a singleton pregnancy who are Latina, who intend to breastfeed for more than 2 months, who have or do not have a history of depression, and who are willing to be followed for 8 weeks after delivery will be enrolled in the study. Latinas who report maternal or infant disorder that may interfere with breastfeeding; those who endorse substance use, and/or who have or have had a psychiatric disorder (e.g., psychosis or serious personality disorders) other than depression or anxiety will be excluded to minimize risk and confounds with the outcomes of interest.

The investigators aim to: Estimate the prevalence of depression in a consecutive cohort of Chinese patients diagnosed with Type 2 Diabetes (T2D) living in areas of China with different socioeconomical affluence Examine patients' awareness of the frequent coexistence of these 2 conditions Analyze the associations between depression and T2D, in particularly the role of metabolic control, socioeconomical status and cognitive-psychological-behavioral factors To document the predisposing, precipitating and perpetuating factors for depression and their interrelationships in Chinese type 2 diabetic patients

A variety of hormones and immune system processes are responsible for how the body responds to illness. This study concentrates on how the hormone cortisol effects the release of immune system factors called cytokines. Cortisol is a hormone produced in the adrenal glands as a response to stimulation from the pituitary gland. Abnormal levels of cortisol have been seen in several diseases such as depression and multiple sclerosis. Cytokines are factors produced by certain white blood cells. They act by changing the cells that produce them (autocrine effect), altering other cells close to them (paracrine), and effecting cells throughout the body (endocrine effect). Cytokines are important in controlling inflammation processes. In this study researchers would like to determine if changes in levels of hormones in the blood are associated with changes in cytokine levels. In addition, researchers would like to learn more about how cytokines respond to hormones in certain diseases.

Investigators are evaluating the use of phone sensor data to estimate behavior, depression and anxiety.

Cognitive deficits in major depression seem explicable by the well-recognized concept of impaired neuroplasticity in mood disorders. This concept initially emerged from preclinical evidence that antidepressants phosphorylate and therefore activate the cyclic AMP response element binding protein (CREB) that is essential for synaptic plasticity. Nevertheless, the question remains whether the activation of CREB by antidepressants is relevant for the remission of cognitive deficits in patients. We addressed this issue by investigating the cognitive improvement during treatment with either citalopram or reboxetine because these antidepressants are different in their capacity to increase phosphorylated CREB (pCREB). Besides the pharmacological treatment groups, another group of patients was treated exclusively with psychotherapy.

This study will evaluate a possible tool for predicting future effectiveness of bright light in treating seasonal affective disorder, winter subtype, and will examine secondary effects of bright light on cardiovascular risk factors.

This study will examine whether spring and fall seasonal depression in individuals with high sensitivity to pollen is linked to seasonal increases in tree and ragweed pollen.