Bondy Brigitta
Psychiatric Hospital, University of Munich, Germany.
Dialogues Clin Neurosci. 2007;9(1):19-28. doi: 10.31887/DCNS.2007.9.1/bbondy.
There is increasing knowledge regarding the considerable comorbidity between depression and cardiovascular disease, which are two of the most common disorders in developed countries. The associated vulnerability is not unidirectional, as the presence of cardiovascular disease can also influence mood states. Although this may be the result of psychological factors, common biological mechanisms, including genetic ones, are thought to be responsible for this interaction; we can thus question whether variations in genes could be predisposing factors. Regarding the multiple interactions in the mechanisms between depression and cardiovascular system disorders, e.g., dysfunctions in the hypothalamic-pituitary-adrenocortical and sympathoadrenal axis and the response to stress, the importance of the serotonergic and immune systems, or the impact on the renin-angiotensin system, several candidate genes are being investigated. However, despite the interest in unraveling the potential susceptibility genes for both disorders, most available studies have so far dealt with the impact of polymorphisms in relation to either depression or cardiovascular disease. A few recent studies have now examined the effects of gene-gene or gene-environment interactions, and are investigating the impact of "depression-related" variants on cardiac response to stress. The first promising results were obtained with the serotonin transporter, and it may be hypothesized that this polymorphism interacts via the impact of the S allele on depression and via the effect of the L allele on platelet activation. However, the role played by various other candidate genes remains to be determined, especially regarding the question as to whether they are indicative of common pathophysiological mechanisms, or for identifying a subgroup of patients with somatic disorders that are more closely related to psychiatric symptoms.
关于抑郁症与心血管疾病之间存在显著共病的认识日益增加,这两种疾病是发达国家最常见的两种疾病。这种关联的易感性并非单向的,因为心血管疾病的存在也会影响情绪状态。尽管这可能是心理因素的结果,但包括遗传因素在内的常见生物学机制被认为是这种相互作用的原因;因此,我们可以质疑基因变异是否可能是易感因素。关于抑郁症与心血管系统疾病之间机制的多种相互作用,如下丘脑 - 垂体 - 肾上腺皮质和交感肾上腺轴功能障碍以及对压力的反应、血清素能和免疫系统的重要性,或对肾素 - 血管紧张素系统的影响,正在研究几个候选基因。然而,尽管人们对揭示这两种疾病的潜在易感基因很感兴趣,但迄今为止,大多数现有研究都只涉及多态性与抑郁症或心血管疾病其中之一的关系。最近有一些研究现在已经研究了基因 - 基因或基因 - 环境相互作用的影响,并正在研究“抑郁症相关”变异对心脏应激反应的影响。血清素转运体已取得了首个有前景的结果,可以推测这种多态性通过S等位基因对抑郁症的影响以及L等位基因对血小板活化的影响相互作用。然而,其他各种候选基因所起的作用仍有待确定,特别是关于它们是否指示共同的病理生理机制,或者用于识别与精神症状更密切相关的躯体疾病患者亚组的问题。