View clinical trials related to Involutional Depression.
Filter by: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.
A series of studies in patients with major depression have consistently demonstrated a doubling of the mortality rate at any age, independent of suicide. In addition, the relative risk for clinically significant coronary artery disease in patients with major depression is also 2 or more in studies that independently controlled for risk factors such as smoking, hypertension, etc. The principal long-term goals of the CNE include the determination of the mechanisms that underlie enhanced susceptibility to premature ischemic heart disease in patients with major depression, documenting the age at which demonstrable pathophysiologic or predictive changes begin to occur, and charting their rate of progression. Our long-term goal is to use our understanding of underlying mechanisms to enhance our capacity to predict who with major depression is most likely to develop premature ischemic heart disease, to determine what the mechanisms underlying this susceptibility are, and to develop improved means for treatment and prevention. Depressed patients are known to manifest a variety of neuroendocrine changes that predispose to coronary artery disease including hypercortisolism, decreased secretion of growth hormone and a deficiency of sex steroids. A final common denominator of these neuroendocrine abnormalities is insulin resistance. Insulin resistance promotes several changes that would favor hypertension and increased coronary artery disease including increased sodium retention, increased activity of the sympathetic nervous system, proliferation of vascular smooth muscle and deposition of highly metabolically active visceral fat. The latter induces additional risk factors for coronary disease, including dyslipidemia, hypercoagulation, and enhanced inflammation. It is a matter of public health importance to document the frequency and severity of insulin resistance in patients with major depression compared to a closely matched group of healthy controls. To accurately quantify insulin resistance in each patient and control, we will apply the hyperinsulinemic euglycemic glucose clamp procedure. This is the gold standard method for measuring the insulin sensitivity since it reflects the direct human body glucose metabolic response to a known insulin infusion. Moreover, it is essential to use this technique in patients with major depression as data indicate that other alternative procedures give unreliable results in the context of hypercortisolism.
This is a study investigating the hormones and substances important to the stress response. The hormone that is most directly responsible for stress response is called corticotropin-releasing hormone (CRH). CRH is produced in the hypothalamus of the brain and causes the pituitary gland to produce another hormone called ACTH. The hormone ACTH then acts on the adrenal glands causing them to produce the hormone cortisol. Unfortunately, CRH levels are unable to be measured in simple blood samples. However, substances like cortisol and leptin can provide information as to the activity of the hypothalamus. The hormone leptin is associated with the regulation of body weight and the normal maintenance of bodily functions (homeostasis). It is found in fat cell (adipocyes) and communicates the nutritional status of the body to the brain (central nervous system). Research using animals has shown that defects in the communication between leptin and the brain causes obesity (the state of being overweight). It has also been noted that obese humans tend to have high levels of leptin. By studying patients with abnormal genes responsible for leptin production, researchers have found that a least one leptin gene must be intact for the normal secretion of hormones to proceed. These results show that the hormone leptin is produced outside of the brain in fat cells and acts directly on the function of the hypothalamus within the brain. Researchers believe that leptin plays a key role in the normal release of hormones from the HPA axis. Researchers intend on continuing to study the role of leptin in fat distribution, and the activity of the HPA axis in normal volunteers. In addition, this study will focus on the role of leptin in depression, because depression is characterized by changes in food intake, body weight, and neuroendocrine function. Data gathered from this study will provide a better understanding of the causes and medical consequences of major depression.
The purpose of this study is to examine calcium absorption and bone mineral density in women with depression. Research indicates that pre-menopausal women with depression have significantly lower bone mineral density (BMD) than pre-menopausal women without depression. Although the mechanisms of BMD loss are unclear, researchers believe that individuals with depression have impaired calcium absorption. However, it is unknown whether the abnormal absorption is a result of depression or a side effect of the drugs used to treat it. This study will compare calcium absorption in women with depression and in healthy women without depression. Participants in this study will be given two non-radioactive calcium isotopes. One can be taken by mouth and the other must be injected. Participants will have the level of isotopes in their urine measured to estimate true fractional calcium absorption (TFCA). Participants may also have a dual X-ray absorptiometry (DEXA) scan to measure total body adiposity and lean body mass.
This research study is the continuation of a study started more than 20 years ago. The study was designed to explore the effect that depressed parents have on their children and to better understand the factors that contribute to depression development and maintenance. The study will continue to investigate if children have certain characteristics in early and middle childhood that predict the later development of psychological disorders. In addition, the study will continue looking at the processes responsible for the development of children of parents with and without affective (mood) disorders.
This study will examine the effectiveness of omega-3 fatty acids, compounds found in plants and fish, in treating bipolar disorder. Some studies have indicated that omega-3 fatty acids may be effective in treating mood disorders. For example, one investigator has shown a correlation between the prevalence of major depression and the amount of fish consumed per capita worldwide. Others have found decreased amounts of EPA (one of the active ingredients in omega-3 fatty acids) in the red blood cells of patients with major depression. And a recent small study of patients with bipolar illness indicated that omega-3 fatty acids prevented relapses, especially of depression, in patients. Patients with bipolar disorder who are not benefiting satisfactorily on their current medications are eligible to participate in this study. Candidates will be screened with a psychiatric evaluation, routine blood tests, a urine test and other tests needed to monitor medications. Participants will be randomly assigned to one of two groups: one group will receive 6 grams of omega-3 fatty acid every day for 16 weeks; the second will receive a placebo (inactive capsule). In addition, patients in both groups will continue to take their previous medications. Every 2 weeks, all patients will have their vital signs checked and be evaluated for side effects and mood changes. At the end of the 16-week study period, all patients will be given the opportunity to continue in the study for another 8 months and receive active drug (omega-3 fatty acid). Patients who continue will be evaluated once a month and will have blood drawn on the last visit for routine tests.