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Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation

机译:为什么抑郁患者发炎? 对20年的抑郁症,糖皮质激素抗性和炎症研究的反思

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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. (C) 2017 The Author. Published by Elsevier B.V.
机译:过去20年的研究表明,下丘脑 - 垂体 - 肾上腺(HPA)轴的炎症和多动是主要抑郁症中最一致的生物学发现中的两个,并且通常是相关的:但是这些异常的分子和临床机制是还不清楚。这些发现特别神奇,特别是考虑到高水平的皮质醇具有抗炎作用的所接受的观念,因此同一诊断组中炎症和高菌血症的共存似乎是反直观的。为了庆祝我们的实验室的2015年Anna-Monika基金会奖,本综述将讨论我们自己的20年对临床和分子证据进行抑郁症炎症增加的临床和分子证据的研究,尤其是在过度活跃的HPA轴的背景下,并讨论其影响对于这种疾病的发病机制和治疗。 (c)2017年作者。 elsevier b.v出版。

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