Psychology Department, Binghamton University-SUNY, Binghamton, NY 13902-6000, USA.
Cogn Emot. 2013;27(2):193-216. doi: 10.1080/02699931.2012.712950. Epub 2012 Aug 24.
There is growing interest in integrating cognitive and genetic models of depression risk. We review two ways in which these models can be meaningfully integrated. First, information-processing biases may represent intermediate phenotypes for specific genetic influences. These genetic influences may represent main effects on specific cognitive processes or may moderate the impact of environmental influences on information-processing biases. Second, cognitive and genetic influences may combine to increase reactivity to environmental stressors, increasing risk for depression in a gene×cognition×environment model of risk. There is now growing support for both of these ways of integrating cognitive and genetic models of depression risk. Specifically, there is support for genetic influences on information-processing biases, particularly the link between 5-HTTLPR and attentional biases, from both genetic association and gene×environment (G×E) studies. There is also initial support for gene×cognition×environment models of risk in which specific genetic influences contribute to increased reactivity to environmental influences. We review this research and discuss important areas of future research, particularly the need for larger samples that allow for a broader examination of genetic and epigenetic influences as well as the combined influence of variability across a number of genes.
人们对整合抑郁风险的认知和遗传模型越来越感兴趣。我们回顾了这两种模型可以有意义地整合的两种方式。首先，信息处理偏差可能代表特定遗传影响的中间表型。这些遗传影响可能代表对特定认知过程的主要影响，也可能调节环境影响对信息处理偏差的影响。其次，认知和遗传影响可能结合起来增加对环境应激源的反应性，从而在抑郁的基因×认知×环境风险模型中增加抑郁的风险。现在，越来越多的人支持将认知和遗传模型整合起来研究抑郁风险。具体来说，遗传关联和基因×环境（G×E）研究都支持遗传对信息处理偏差的影响，特别是 5-HTTLPR 与注意偏差之间的联系。对于风险的基因×认知×环境模型也有初步支持，其中特定的遗传影响会导致对环境影响的反应性增加。我们回顾了这项研究，并讨论了未来研究的重要领域，特别是需要更大的样本量，以便更广泛地研究遗传和表观遗传影响以及许多基因的变异性的综合影响。
