Elevated immune-inflammatory signaling in mood disorders: a new therapeutic target?
Elevated immune-inflammatory signaling in mood disorders: a new therapeutic target?
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DOI：
10.1586/ern.12.98
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发表时间：
2012-09
影响因子：
4.3
通讯作者：
Lotrich FE
中科院分区：
文献类型：
--
作者：
McNamara RK;Lotrich FE
汇聚翻译证据暗示情绪障碍，包括重度抑郁症和双相情感障碍的病理学中的免疫炎症信号传导活性升高。这部分得到了横截面证据的支持，即情绪发作期间促炎性类花生酸、细胞因子和急性期蛋白水平增加，以及慢性免疫炎症激活引起情绪症状出现的前瞻性纵向证据。此外，情绪稳定剂和非典型抗精神病药物下调免疫炎症信号通路的初始组分，并且用抗炎剂连续治疗增加了抗抑郁药、情绪稳定剂和非典型抗精神病药物的疗效。与升高的免疫炎症信号相关的潜在致病机制包括中枢5-羟色胺神经传递的扰动和进行性白色物质病理学。遗传遗传因素和环境因素（包括膳食脂肪酸组成）可能共同作用，维持免疫炎症信号的升高。总的来说，这些数据表明，升高的免疫炎症信号传导是一种与情绪障碍的病理学相关的机制，因此可能代表了开发更有效治疗方法的新的治疗靶点。
Converging translational evidence has implicated elevated immune-inflammatory signaling activity in the pathoetiology of mood disorders, including major depressive disorder and bipolar disorder. This is supported in part by cross-sectional evidence for increased levels of proinflammatory eicosanoids, cytokines and acute-phase proteins during mood episodes, and prospective longitudinal evidence for the emergence of mood symptoms in response to chronic immune-inflammatory activation. In addition, mood-stabilizer and atypical antipsychotic medications downregulate initial components of the immune-inflammatory signaling pathway, and adjunctive treatment with anti-inflammatory agents augment the therapeutic efficacy of antidepressant, mood stabilizer and atypical antipsychotic medications. Potential pathogenic mechanisms linked with elevated immune-inflammatory signaling include perturbations in central serotonin neurotransmission and progressive white matter pathology. Both heritable genetic factors and environmental factors including dietary fatty-acid composition may act in concert to sustain elevated immune-inflammatory signaling. Collectively, these data suggest that elevated immune-inflammatory signaling is a mechanism that is relevant to the pathoetiology of mood disorders, and may therefore represent a new therapeutic target for the development of more effective treatments.
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