Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation
Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these...
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| Published in | European neuropsychopharmacology Vol. 27; no. 6; pp. 554 - 559 |
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| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.06.2017
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these abnormalities are still unclear. These findings are particularly enigmatic, especially considering the accepted notion that high levels of cortisol have an anti-inflammatory action, and therefore the coexistence of inflammation and hypercortisolemia in the same diagnostic group appears counter-intuitive. To celebrate the 2015 Anna-Monika Foundation Award to our laboratory, this review will discuss our own 20 years of research on the clinical and molecular evidence underlying the increased inflammation in depression, especially in the context of a hyperactive HPA axis, and discuss its implications for the pathogenesis and treatment of this disorder. |
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| AbstractList | Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these abnormalities are still unclear. These findings are particularly enigmatic, especially considering the accepted notion that high levels of cortisol have an anti-inflammatory action, and therefore the coexistence of inflammation and hypercortisolemia in the same diagnostic group appears counter-intuitive. To celebrate the 2015 Anna-Monika Foundation Award to our laboratory, this review will discuss our own 20 years of research on the clinical and molecular evidence underlying the increased inflammation in depression, especially in the context of a hyperactive HPA axis, and discuss its implications for the pathogenesis and treatment of this disorder. Abstract Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these abnormalities are still unclear. These findings are particularly enigmatic, especially considering the accepted notion that high levels of cortisol have an anti-inflammatory action, and therefore the coexistence of inflammation and hypercortisolemia in the same diagnostic group appears counter-intuitive. To celebrate the 2015 Anna-Monika Foundation Award to our laboratory, this review will discuss our own 20 years of research on the clinical and molecular evidence underlying the increased inflammation in depression, especially in the context of a hyperactive HPA axis, and discuss its implications for the pathogenesis and treatment of this disorder. Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these abnormalities are still unclear. These findings are particularly enigmatic, especially considering the accepted notion that high levels of cortisol have an anti-inflammatory action, and therefore the coexistence of inflammation and hypercortisolemia in the same diagnostic group appears counter-intuitive. To celebrate the 2015 Anna-Monika Foundation Award to our laboratory, this review will discuss our own 20 years of research on the clinical and molecular evidence underlying the increased inflammation in depression, especially in the context of a hyperactive HPA axis, and discuss its implications for the pathogenesis and treatment of this disorder.Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis are two of the most consistent biological findings in major depression and are often associated: but the molecular and clinical mechanisms underlying these abnormalities are still unclear. These findings are particularly enigmatic, especially considering the accepted notion that high levels of cortisol have an anti-inflammatory action, and therefore the coexistence of inflammation and hypercortisolemia in the same diagnostic group appears counter-intuitive. To celebrate the 2015 Anna-Monika Foundation Award to our laboratory, this review will discuss our own 20 years of research on the clinical and molecular evidence underlying the increased inflammation in depression, especially in the context of a hyperactive HPA axis, and discuss its implications for the pathogenesis and treatment of this disorder. |
| Author | Pariante, Carmine M. |
| Author_xml | – sequence: 1 givenname: Carmine M. surname: Pariante fullname: Pariante, Carmine M. email: Carmine.Pariante@kcl.ac.uk organization: Stress, Psychiatry and Immunology Laboratory (SPI-Lab), Stress, Psychiatry and Immunology Lab & Perinatal Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King׳s College London, G.32.01, The Maurice Wohl Clinical Neuroscience Institute, Cutcombe Road, London SE5 9RT, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28479211$$D View this record in MEDLINE/PubMed |
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| Issue | 6 |
| Keywords | Immunopsychiatry Antidepressants Glucocorticoid receptor HPA mRNA Psychoneuroimmunology Childhood trauma |
| Language | English |
| License | This is an open access article under the CC BY license. Copyright © 2017 The Author. Published by Elsevier B.V. All rights reserved. |
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| Snippet | Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis are two of the... Abstract Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis are... Studies over the last 20 years have demonstrated that increased inflammation and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis are two of the... |
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| SubjectTerms | Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - therapeutic use Antidepressants Biomedical Research - trends Childhood trauma Depression - drug therapy Depression - metabolism Depression - psychology Glucocorticoid receptor Glucocorticoids - metabolism Glucocorticoids - therapeutic use HPA Humans Hydrocortisone - metabolism Hypothalamo-Hypophyseal System - metabolism Immunopsychiatry Inflammation - drug therapy Inflammation - metabolism Inflammation - psychology Inflammation Mediators - metabolism Internal Medicine Metabolism, Inborn Errors - drug therapy Metabolism, Inborn Errors - metabolism Metabolism, Inborn Errors - psychology mRNA Pituitary-Adrenal System - metabolism Psychiatry Psychoneuroimmunology Receptors, Glucocorticoid - deficiency Receptors, Glucocorticoid - metabolism Time Factors |
| Title | Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation |
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