Topic
Endogenous depression
About: Endogenous depression is a research topic. Over the lifetime, 2490 publications have been published within this topic receiving 87862 citations. The topic is also known as: clinical depression & unipolar depression.
Papers published on a yearly basis
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Papers
TL;DR: The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone.
Abstract: Depression is a multicausal disorder and has been associated with the risk to develop cancer, dementia, diabetes, epilepsy and stroke. As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. As a cardiovascular disease a close relationship exists between depression and blood pressure, heart rate, norepinephrine, sympathetic tone, vascular resistance, blood viscosity, plasma volume, intima thickness and atherosclerosis. Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. Nutritional factors might influence depression risk, i.e. the consumption of folate, omega-3 fatty acids, monounsaturated fatty acids, olive oil, fish, fruits, vegetables, nuts, legumes, vitamin B6 and vitamin B12. The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. In this context, a fast neuroprotective and antidepressant effect has also been observed by ketamine, which acts via the glutamatergic system. Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. Alternative, causative or also easy available treatment strategies beyond serotonin and noradrenaline reuptake inhibition might be a major topic of future psychiatric care. In this review, an attempt is made to overview concepts of the disease and search for perspectives on antidepressant treatment strategies beyond approved medications.
8,092 citations
TL;DR: Abnormal DST results were found with similar frequency among outpatients and inpatients with melancholia; but they were not related to age, sex, recent use of psychotropic drugs, or severity of depressive symptoms.
Abstract: • Four hundred thirty-eight subjects underwent an overnight dexamethasone suppression test (DST) to standardize the test for the diagnosis of melancholia (endogenous depression). Abnormal plasma cortisol concentrations within 24 hours after dexamethasone administration occurred almost exclusively in melancholic patients. The best plasma cortisol criterion concentration, above which a DST result may be considered abnormal, was 5 ug/dL. The optimal dose of dexamethasone was 1 rather than 2 mg. Two blood samples obtained at 4 and 11 PM after dexamethasone administration detected 98% of the abnormal test results. This version of the DST identified melancholic patients with a sensitivity of 67% and a specificity of 96%. Baseline nocturnal plasma cortisol concentrations were not useful. Abnormal DST results were found with similar frequency among outpatients and inpatients with melancholia; but they were not related to age, sex, recent use of psychotropic drugs, or severity of depressive symptoms. Extensive evidence validates this practical test for the diagnosis of melancholia.
2,243 citations
TL;DR: This review presents the major current approaches to understanding the biologic mechanisms of major depression and defines depression as a heterogeneous disorder with a highly variable course, an inconsistent response to treatment, and no established mechanism.
Abstract: Depression is related to the normal emotions of sadness and bereavement, but it does not remit when the external cause of these emotions dissipates, and it is disproportionate to their cause. Classic severe states of depression often have no external precipitating cause. It is difficult, however, to draw clear distinctions between depressions with and those without psychosocial precipitating events. 1 The diagnosis of major depressive disorder requires a distinct change of mood, characterized by sadness or irritability and accompanied by at least several psychophysiological changes, such as disturbances in sleep, appetite, or sexual desire; constipation; loss of the ability to experience pleasure in work or with friends; crying; suicidal thoughts; and slowing of speech and action. These changes must last a minimum of 2 weeks and interfere considerably with work and family relations. On the basis of this broad definition, the lifetime incidence of depression in the United States is more than 12% in men and 20% in women. 2 Some have advocated a much narrower definition of severe depression, which they call melancholia or vital depression. 3 A small percentage of patients with major depression have had or will have manic episodes consisting of hyperactivity, euphoria, and an increase in pleasure seeking. Although some pathogenetic mechanisms in these cases and in cases of major depressive disorder overlap, a history of mania defines a distinct illness termed bipolar disorder. 4 Depression is a heterogeneous disorder with a highly variable course, an inconsistent response to treatment, and no established mechanism. This review presents the major current approaches to understanding the biologic mechanisms of major depression.
2,072 citations
TL;DR: This work has shown that antagonists designed to directly target molecules in signaling pathways that regulate neuroplasticity and cell survival in major depressive disorders may hold promise as new therapeutics for depression.
Abstract: Major depressive disorders, long considered to be of neurochemical origin, have recently been associated with impairments in signaling pathways that regulate neuroplasticity and cell survival. Agents designed to directly target molecules in these pathways may hold promise as new therapeutics for depression.
1,249 citations
TL;DR: In this paper, a comprehensive review of the relationship between sleep and depression is presented, focusing on the relationships between sleep disturbance and depression, and focusing on sleep-related hypotheses explaining the pathophysiology of depression.
Abstract: Background Of all the psychiatric disorders associated with insomnia, depression is the most common. It has been estimated that 90% of patients with depression complain about sleep quality. Since the first reports of short rapid eye movement (REM) latency in depressed patients and of the effect of sleep deprivation on depression in the 1970s, numerous sleep studies have provided extensive observations and theoretical hypotheses concerning the etiology and pathophysiology of depression. The aim of this review is to summarize knowledge regarding the relationships between sleep and depression. Data sources and selection MEDLINE and PsycINFO searches of the literature published in English or French between 1964 and 2005 that examined the relationships between sleep disturbance and depression were conducted. Search terms used were depression, depressive disorder, affective disorder, mood disorders, seasonal affective disorder, sleep, sleep disorders, insomnia, REM, polysomnography, sleep deprivation, electroencephalography, PET, SPECT, and fMRI. Data synthesis Two hundred five papers were identified and selected and then integrated into the following categories: sleep architecture, antidepressive therapies, age- and gender-associated differences, functional imaging results, and sleep-related hypotheses explaining the pathophysiology of depression. Conclusion Numerous studies provide findings indicating the remarkable relationship between sleep alterations and depression. Although the existing hypotheses are not likely to explain all aspects of the sleep alterations in depression, each may be worth being maintained for refinements of pathophysiologic models of depression as new data accumulate. Further research taking into account the heterogeneity of depressive disorder and linking the different areas of research is needed to develop more comprehensive theoretical models and new therapies for depression.
1,044 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2024 | 1 |
| 2023 | 1 |
| 2022 | 3 |
| 2021 | 10 |
| 2020 | 5 |
| 2019 | 5 |