Inflammation and depression: Research designs to better understand the mechanistic relationships between depression, inflammation, cognitive dysfunction, and their shared risk factors.
Inflammation and depression: Research designs to better understand the mechanistic relationships between depression, inflammation, cognitive dysfunction, and their shared risk factors.
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DOI：
10.1016/j.bbih.2021.100278
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发表时间：
2021-08
期刊：
影响因子：
--
通讯作者：
Mac Giollabhui N
中科院分区：
文献类型：
--
作者：
Mac Giollabhui N
有证据表明，免疫系统在一些抑郁症患者中失调。一个基于心理神经免疫学的抑郁症的理解正在迅速推进，然而，一个基本的重要性的问题是知之甚少：炎症是否在抑郁症的病因学中发挥因果作用，或者升高的炎症生物标志物是抑郁行为的下游效应？虽然纵向研究表明，抑郁症和炎症之间的关系的特点是复杂的双向协会，现有的前瞻性，纵向研究设计的装备不足，以调查抑郁症和炎症的动态相互作用，在一个相对较短的时间内展开。此外，多重、共享和重叠的风险因素（例如，饮食、肥胖、压力、睡眠失调）在抑郁症病因学中的作用以及促炎表型（或两者）的作用知之甚少。在这篇手稿中，我强调了研究设计的好处，（i）使用干预或治疗设计操纵感兴趣的结构（抑郁/炎症），（ii）使用密集的采样方法，最终目标是更好地理解抑郁症，炎症，认知功能障碍及其共同风险因素的时间顺序和因果关系。例如，抑郁症状的改善是运动增加引起的炎症活动变化的下游效应，还是运动增加引起的睡眠质量改善引起的炎症活动变化和抑郁后遗症？这些研究设计的潜在好处进行了讨论，在他们的贡献，以更好地了解抑郁症的病因和促炎表型，其相关性的结构性健康不平等，更好地表征抑郁症的异质性临床表现，特别是有关抑郁症的认知功能障碍的病因。炎症在抑郁症的病因学中起着因果作用（以及相反）的证据进行了审查。抑郁症和炎症之间的因果关系尚不清楚，因为有多种，共享和重叠的风险因素。探讨抑郁症、炎症和认知功能障碍的因果关系的方法。
There is convergent evidence that the immune system is dysregulated in some depressed individuals. A psychoneuroimmunology-based understanding of depression is advancing rapidly; however, a question of fundamental importance is poorly understood: does inflammation play a causal role in the etiology of depression or are elevated inflammatory biomarkers a downstream effect of depressive behaviors? Although longitudinal studies suggest that the relationship between depression and inflammation is characterized by complex bidirectional associations, existing prospective, longitudinal research designs are poorly equipped to investigate the dynamic interplay of depression and inflammation that unfolds over a relatively short time period. In addition, the precise role played by multiple, shared, and overlapping risk factors (e.g., diet, adiposity, stress, sleep dysregulation) in the etiology of depression and a pro-inflammatory phenotype (or both) is poorly understood. In this manuscript, I highlight the benefits of research designs that (i) manipulate constructs of interest (depression/inflammation) using intervention or treatment designs and (ii) use intensive sampling approaches with an ultimate goal of better understanding the temporal sequence and causal relationships of depression, inflammation, cognitive dysfunction, and their shared risk factors. For instance, are improved depressive symptoms a downstream effect of changes in inflammatory activity caused by increases in exercise or, alternatively, are changes in inflammatory activity and depression sequelae of improvements in sleep quality caused by increases in exercise? Potential benefits of these research designs are discussed in terms of their contribution to a better understanding of the etiology of depression and a pro-inflammatory phenotype, their relevance to structural health inequalities, and better characterizing the heterogeneous clinical presentation of depression, particularly relating to the etiology of cognitive dysfunction in depression. Evidence that inflammation plays a causal role in the etiology of depression (as well as the reverse) is reviewed. The causal relationship between depression and inflammation is unclear due to multiple, shared, and overlapping risk factors. Approaches to investigate the causal relationships of depression, inflammation, and cognitive dysfunction are discussed.
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期刊：
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