Zunszain Patricia A, Hepgul Nilay, Pariante Carmine M
Department of Psychological Medicine, Institute of Psychiatry, King's College London, UK.
Curr Top Behav Neurosci. 2013;14:135-51. doi: 10.1007/7854_2012_211.
Major depressive disorder (MDD) is a complex illness and it is likely that alterations in several interacting systems underlie its pathogenesis. Numerous hypotheses have been proposed to elucidate its origins. The inflammatory hypothesis emphasises the role of psycho-neuroimmunological dysfunctions. This is based on several observations: subsets of MDD patients have an altered peripheral immune system, with impaired cellular immunity and increased levels of proinflammatory cytokines; cytokines can influence neurotransmitter metabolism, neuroendocrine function and regional brain activity, all of which are relevant to depression; acute administration of cytokines causes sickness behaviour which shares features with depression, and patients undergoing cytokine treatment develop depressive symptoms. In this chapter, we discuss the evidence linking inflammation and MDD, looking at data from clinical and animal studies, the role of stress, possible mechanisms and the involvement of genetic polymorphisms. Further understanding of pathways involved is still needed. This will be vital for the identification of new drug targets and preventative strategies.
重度抑郁症(MDD)是一种复杂的疾病,其发病机制可能涉及多个相互作用系统的改变。人们已经提出了许多假说来阐明其病因。炎症假说强调心理神经免疫功能障碍的作用。这一假说基于以下几点观察:部分MDD患者的外周免疫系统发生改变,细胞免疫受损,促炎细胞因子水平升高;细胞因子可影响神经递质代谢、神经内分泌功能和脑区活动,所有这些都与抑郁症相关;急性给予细胞因子会导致出现与抑郁症相似的疾病行为,接受细胞因子治疗的患者会出现抑郁症状。在本章中,我们将讨论炎症与MDD之间联系的证据,审视来自临床和动物研究的数据、应激的作用、可能的机制以及基因多态性的影响。仍需进一步了解其中涉及的途径。这对于确定新的药物靶点和预防策略至关重要。