Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Galanin (GAL) a 29 amino-acid peptide, is distributed in the central and peripheral nervous system, the pituitary gland, the gastrointestinal tract and also in the endocrine and exocrine pancreas. The endogenous and exogenous effects of galanin are mediated by three receptor subtypes, which are termed: GALR1, GALR2, GALR3. Galanin has a significant role in physiological and pathological processes (acromegally, diarhoea, collitis, Alzheimer's disease, oberitas depression, pituitary gland adenomas) in a human body and animals. It has an ability to contract smooth muscles in gastrointestinal tract, stimulates reflexes in the central nervous system, decreases pancreatic amylase release, changes transport of electrolytes Na+ and Cl-, exerts tonic inhibition of nociceptive input to the central nervous system, stimulates glucagon release, inhibits insulin and somatostatin release, takes part in prolactin secretion, stimulates growth hormone--releasing hormone, hypothalamic gonadotropin releasing hormone and corticotropin releasing hormone. It causes increase of somatotropin secretion, foliculotropin and luteinizing hormone release and adrenocorticotropin secretion.
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PMID:[The significance of galanin in physiologic and pathologic processes in humans]. 1122 78

Hyperresponsiveness of the hypothalamo-pituitary-adrenal (HPA) axis in multiple sclerosis (MS), an autoimmune inflammatory disease of the central nervous system, is presumably due to diminished corticosteroid receptor function. It probably influences the immune response, but its clinical significance is not clear. Similar HPA dysregulation occurs in depression and is reversible with successful antidepressant treatment. We conducted a double blind, placebo-controlled trial to evaluate the neuroendocrine effect of cotreatment with the antidepressant moclobemide as an adjunct to oral corticosteroids in MS. Twenty-one patients with definite relapsing-remitting MS (11 females, aged 33.9 +/- 2.0 yr; Expanded Disability Status Scale score of neurological impairment, 2.0--6.5) in acute relapse were treated with placebo (n = 13) or 300 mg moclobemide (reversible monoamine oxidase A inhibitor; n = 8) for 75 days. All received oral fluocortolone from day 7 on, and the dose was tapered until day 29. Effects were evaluated using the combined dexamethasone-CRH test and clinically on days 1, 30, and 75. At baseline, the HPA axis was mildly activated, comparably for treatment groups [area under the curve for cortisol (AUC-Cort), 213.8 +/- 76.8 arbitrary units in the moclobemide group vs. 225.8 +/- 65.1 in the steroid alone group; mean +/- SEM]. In a group of healthy controls with comparable demographic characteristics, the AUC-Cort was 107.4 +/- 14.1. Moclobemide cotreatment resulted in normalization of the HPA axis response, whereas the HPA system hyperresponse was maintained with steroids alone (AUC-Cort on day 30, 85.9 +/- 22.8 vs.177.1 +/- 68.5; on day 75, 111.0 +/- 46.0 vs. 199.2 +/- 64.6). The change in Expanded Disability Status Scale was comparable for both groups. Although corticosteroids alone had no effect on the HPA response using the dexamethasone-CRH test, treatment with moclobemide combined with corticosteroids favors normalization of the HPA response in relapsing-remitting MS.
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PMID:Combined treatment with corticosteroids and moclobemide favors normalization of hypothalamo-pituitary-adrenal axis dysregulation in relapsing-remitting multiple sclerosis: a randomized, double blind trial. 1129 92

Sleep disturbance and cognitive impairment are frequent complaints of depressed patients under standard antidepressant medication. Therefore, additional therapies are required which specifically focus on the improvement of these deficits without exerting major side effects. Ginkgo biloba extract (EGb) has been shown to improve cognitive abilities in elderly subjects and in patients with disorders of the dementia spectrum. Animal studies surmise that EGb may reduce CRH activity, which is substantially related to depressive mood and behavior, predominantly cognition and sleep. An open non-randomized pilot study has been conducted to investigate the effects of ginkgo biloba extract (EGb Li 1370) on cognitive performance and sleep regulation in depressed inpatients. 16 patients were treated with a trimipramine (T)-monotherapy (200 mg) for six weeks. In eight of the 16 patients, an adjunct EGb therapy (240 mg/d) was applied for four weeks after a baseline week, the other eight patients remained on trimipramine monotherapy (200 mg) during the entire study. Polysomnography, cognitive psychomotor performance and psychopathology were assessed at baseline, after short-term and long-term adjunct EGb treatment, and after one week of ginkgo discontinuation (at the respective evaluation times in the eight patients on T-monotherapy). This report focuses on the results of EGb on sleep EEG pattern. EGb significantly improved sleep pattern by an increase of sleep efficiency and a reduction of awakenings. In addition, sleep stage 1 and REM-density were reduced, while stage 2 was increased. Non-REM sleep, predominantly slow wave sleep in the first sleep cycle, was significantly enhanced compared to trimipramine monotherapy. Discontinuation of EGb reversed most of these effects. Based on the animal data, these results suggest that EGb may improve sleep continuity and enhance Non-REM sleep due to a weakening of tonic CRH-activity. The compensation of the deficient Non-REM component in depression by the EGb application may provide a new additional treatment strategy, especially in the treatment of the depressive syndrome with sleep disturbance.
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PMID:Polysomnographic effects of adjuvant ginkgo biloba therapy in patients with major depression medicated with trimipramine. 1130 64

The development and course of depression is causally linked to impairment of central regulation of the hypothalamic-pituitary-adrenocortical (HPA) system. Previous research documented that the combined dexamethasone/corticotropin-releasing hormone (DEX/CRH) test identifies HPA dysfunction with high sensitivity. We evaluated the predictive validity for medium-term outcome of the cortisol response in the combined DEX/CRH test in 74 remitted patients previously suffering from major depressive disorder. Of the 74 patients, 61 remained in stable remission and 13 relapsed during the first 6 months after discharge from the hospital. Although the cortisol and ACTH responses in the DEX/CRH test did not differ between the two groups of patients on admission, the responses differed significantly just before discharge (P< 0.05). We defined two dichotomous variables as prediction rules indicating (1) the change between admission and discharge in the cortisol response to the DEX/CRH test, and (2) the effect of the CRH infusion on cortisol as compared to the baseline level in the DEX/CRH test prior to discharge only. An elevated cortisol response in the DEX/CRH test was correlated with a four- to six-fold higher risk for relapse than in individuals with a normal cortisol response. The two proposed rules for predicting relapse within the first 6 months after discharge could be optimized by including age and gender. Hence, an exaggerated cortisol response in the combined DEX/CRH test predicts the recurrence of depressive psychopathology. The test performance can be further optimized if gender and age are taken into account.
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PMID:Cortisol response in the combined dexamethasone/CRH test as predictor of relapse in patients with remitted depression. a prospective study. 1137 37

A new subtype of depression is proposed, named: anxiety/aggression-driven depression. The psychopathological, psychopharmacological and biochemical evidence on which this construct is based, is being discussed. Selective postsynaptic 5-HT1A agonists together with CRH and/or cortisol antagonists are hypothesized to be a specific biological treatment for this depression type, in conjunction with psychological interventions to raise the stressor-threshold and to increase coping skills. The development of this depression construct has been contingent on the introduction of two new diagnostic procedures, called functionalization and verticalization of psychiatric diagnosis. These procedures are explained and it is stressed that they are essential to psychiatric diagnosing, in order to put this process on a scientific footing.
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PMID:Anxiety/aggression--driven depression. A paradigm of functionalization and verticalization of psychiatric diagnosis. 1138 84

This paper reviews prior research studies examining neurobiological correlates and treatment response of depression in children, adolescents, and adults. Although there are some similarities in research findings observed across the life cycle, both children and adolescents have been found to differ from depressed adults on measures of basal cortisol secretion, corticotropin stimulation post-corticotropin releasing hormone (CRH) infusion, response to several serotonergic probes, immunity indices, and efficacy of tricyclic medications. These differences are proposed to be due to 1) developmental factors, 2) stage of illness factors (e.g., number of episodes, total duration of illness), or 3) heterogeneity in clinical outcome (e.g., recurrent unipolar course vs. new-onset bipolar disorder). Relevant clinical and preclinical studies that provide support for these alternate explanations of the discrepant findings are reviewed, and directions for future research are discussed. To determine whether child-, adolescent-, and adult-onset depression represent the same condition, it is recommended that researchers 1) use the same neuroimaging paradigms in child, adolescent, and adult depressed cohorts; 2) carefully characterize subjects' stage of illness; and 3) conduct longitudinal clinical and repeat neurobiological assessments of patients of different ages at various stages of illness. In addition, careful attention to familial subtypes (e.g., depressive spectrum disorders vs. familial pure depressive disorders) and environmental factors (e.g., trauma history) are suggested for future investigations.
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PMID:Are child-, adolescent-, and adult-onset depression one and the same disorder? 1143 Aug 41

It is characterized by mainly depressive mood and psychomotor retardation. Another symptoms are retardation of thought, diurnal change, anxiety, irritability, delusion of belittlement, etc. There are often somatic symptoms as loss of appetite, sleep disturbance, loss of body weight, constipation, etc. Depressive symptoms are often seen in schizophrenia, brain injury, endocrinosis illness and other somatic illness. Diagnosis of depression is carefully carried out by detailed interviews and symptoms. Recently diagnosis of depression is determined mechanically by DSM-IV or ICD-10. Neuro-endocrine tests as DST or Dex-CRH test, are useful strategies in examination of depression.
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PMID:[Symptomatology and diagnosis of depression]. 1151 47

Retrospective studies in humans suggest that chronic maternal stress during pregnancy, associated with raised plasma levels of CRH, ACTH and cortisol may increase the likelihood of preterm birth, developmental delays and behavioural abnormalities in the children. In adulthood, it may contribute to the significant association between the incidence of schizophrenia, increased left or mixed handedness, reduction in cerebral asymmetry and anomalies in brain morphology. Our studies and others have shown that prenatal stress in rats can mimic these developmental and behavioural alterations. These rats show a reduced propensity for social interaction, increased anxiety in intimidating or novel situations and a reduction in cerebral asymmetry and dopamine turnover, consistent with those in schizophrenic humans. Prenatally-stressed (PS) rats also show behaviour consistent with depression, including a phase-shift in their circadian rhythm for corticosterone, sleep abnormalities, a hedonic deficit and greater acquisition of learned helplessness under appropriate conditions. These behavioural abnormalities are associated with impaired regulation of the hypothalamic-pituitary-adrenal axis response to stress and increased CRH activity. PS males may show demasculinisation and feminisation of their sexual behaviour. The developmental and behavioural abnormalities in PS offspring could occur through sensitisation of the foetal brain by maternal stress hormones to the action of glucocorticoid and CRH and to neurotransmitters affected by them. This may have long-lasting consequences and could explain the precipitation of depressive symptoms or schizophrenia by psychosocial stress in later life. The character of the behavioural abnormalities probably depends on the timing of the maternal stress in relation to development of the particular neuronal systems.
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PMID:Alterations induced by gestational stress in brain morphology and behaviour of the offspring. 1168 80

Hypothalamo-pituitary-adrenal (HPA) axis is a very complicated control system playing an important role in stress reaction, where glucocorticoids suppress the autonomic (vegetative), endocrine, immunologic and psychic responses to stressful stimuli. We described the marked clinical, physiological, and biochemical connection between osteoporosis and major depressive disorder (MDD). Both conditions are associated with a hyperactive HPA axis and LC/NE system, and hence with increased CRH, cortisol, and catecholamine secretion. There are numerous states or diseases associated with osteoporosis and we were looking for a hypercorticism value as a one of these. Some recent studies demonstrated that earlier history of MDD was associated with marked osteoporosis. In MDD there are two well-documented biochemical abnormalities: hypercortisolism and its resistance to dexamethasone suppression. The present study included 31 MDD patients (19 males and 12 females, mean age 37 +/- 1.3, age range 29-41 years), and 17 healthy male volunteers (mean age 39 +/- 1.6, age range 34-45 years). In each of our patients 24-hour urinary free cortisol, serum cortisol level at 8 a.m. and 5 p.m., cortisol in dexamethasone suppression test and bone mineral density were measured. We have, therefore, analyzed a group of young men and women with normal menstrual cycles, who were without signs of osteoporosis in the beginning, and who received anti-depressive therapy for many years. Analysis showed that increased levels of cortisol and the occurrence of osteoporosis, that developed as the result of elevated cortisol level. For our workshop we used nonparametric rang-correlation with Spearman's rho = -0.805, with statistic significant at the 0.01 level (2-tailed). Patients under long-term history of depression could develop a very stronger type of osteoporosis i.e. it is before known that the patients with untreated Cushing syndrome developed hard osteoporosis.
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PMID:Depressive disorder as possible risk factor of osteoporosis. 1181 Dec 78

The combined dexamethasone/corticotropin releasing hormone (Dex/CRH) test is one of the most reliable neuroendocrine function tests for investigation of hypothalamic-pituitary-adrenocortical (HPA) system dysregulation in depression. Persistent high HPA system activity reflected by an enhanced cortisol secretion during the Dex/CRH test after successful antidepressant treatment is correlated with an enhanced risk for relapse in remitted depressives. Thus, the Dex/CRH test might be a useful neuroendocrinological tool for treatment monitoring. However, the performance of the test requiring multiple blood samplings renders this test difficult for routine clinical use. Thus, a simplified test procedure using a saliva based test without the necessity of multiple blood samplings would be desirable.Therefore, we compared matched saliva and serum probes of Dex/CRH tests of 73 depressed patients who underwent a total of 157 tests. Both saliva and serum cortisol concentrations showed a significant stimulation pattern during the test and were highly correlated. This correlation was not influenced by either antidepressive treatment. In patients with high cortisol secretion patterns during the Dex/CRH test there was a decrease in HPA system activity after successful antidepressant treatment that was reflected by both the saliva and the serum Dex/CRH test.Thus, the saliva based combined Dex/CRH test appears to be a suitable tool for monitoring HPA system activity during the course of depressive illness. The easier performance of the saliva Dex/CRH test in comparison to the standard test procedure for both patients and hospital staff opens the door for routine clinical use of the Dex/CRH test for treatment monitoring and estimation of relapse risk.
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PMID:Evaluation of a salivary based combined dexamethasone/CRH test in patients with major depression. 1181 73


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