Department of Psychiatry, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.
Curr Opin Psychiatry. 2011 Nov;24(6):519-25. doi: 10.1097/YCO.0b013e32834b9db6.
As the 'monoamine hypothesis of depression' fails to explain all aspects of major depression, additional causes are being investigated. Several observations suggest that inflammatory mechanisms pay a role in the cause of major depressive disorder (MDD). This article reviews their role in major depression.
Recent studies support the concept that inflammatory mechanisms play a crucial role in the pathomechanisms of major depression. Major depression shares similarities with 'sickness behavior', a normal response to inflammatory cytokines. Elevations in proinflammatory cytokines and other inflammation-related proteins in major depression were found in plasma and cerebrospinal fluid (CSF) as well as in postmortem studies. Elevated levels of proinflammatory cytokines persist after clinical symptoms of depression are in remission and can also predict the onset of a depressive episode. Antidepressant treatment can lead to a normalization of elevated cytokine levels in major depression. Finally, we understand how inflammatory mechanisms affect the metabolism of tryptophan and how nonsteroidal antiinflammatory drugs (NSAIDs) can interfere with the effects of antidepressants.
Further studies are needed to fully understand the role of inflammatory mechanisms in major depression and the potential treatment implications.
由于“单胺假说”无法解释抑郁症的所有方面，因此正在研究其他病因。一些观察结果表明，炎症机制在重度抑郁症（MDD）的发病机制中起作用。本文综述了其在重度抑郁症中的作用。
最近的研究支持这样一种观点，即炎症机制在重度抑郁症的发病机制中起着至关重要的作用。重度抑郁症与“疾病行为”（对炎症细胞因子的正常反应）具有相似性。在重度抑郁症患者的血浆和脑脊液（CSF）以及尸检研究中发现促炎细胞因子和其他与炎症相关的蛋白质升高。在抑郁症状缓解后，促炎细胞因子的水平仍升高，并可预测抑郁发作的发生。抗抑郁治疗可使重度抑郁症中升高的细胞因子水平恢复正常。最后，我们了解了炎症机制如何影响色氨酸的代谢，以及非甾体抗炎药（NSAIDs）如何干扰抗抑郁药的作用。
需要进一步研究以充分了解炎症机制在重度抑郁症中的作用及其潜在的治疗意义。
