Burmeister Margit, Sen Srijan
Computational Medicine & Bioinformatics and a Research Professor in the Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, USA. She also holds appointments as Professor of Psychiatry and Professor of Human Genetics. She received her doctorate from the Ruprecht Karl University of Heidelberg in Germany for work at the European Molecular Biology Laboratory. She trained as a postdoctoral fellow at the University of California in San Francisco. She has held visiting Professorships at the Max Planck Institute for Molecular Genetics in Berlin, Shanghai Jiao Tong University, China, the Weizmann Institute of Science, Israel, the University of Heidelberg and the Chinese University of Hong Kong in Shenzhen, China.
University of Michigan Depression Center and the Frances and Kenneth Eisenberg Professor of Depression and Neurosciences in the Department for Psychiatry, University of Michigan, Ann Arbor, MI, USA. He is also Associate Vice President for Health Sciences, Research Professor of the Michigan Neuroscience Institute and Professor for Computational Medicine & Bioinformatics at the University of Michigan. He received his MD and PhD at the University of Michigan and trained as resident in psychiatry at Yale University.
BJPsych Adv. 2021 May;27(3):153-157. doi: 10.1192/bja.2021.21. Epub 2021 Apr 23.
Stress is the most important proximal precipitant of depression, yet most large genome-wide association studies (GWAS) do not include stress as a variable. Here, we review how gene × environment (G × E) interaction might impede the discovery of genetic factors, discuss two examples of G × E interaction in depression and addiction, studies incorporating high-stress environments, as well as upcoming waves of genome-wide environment interaction studies (GWEIS). We discuss recent studies which have shown that genetic distributions can be affected by social factors such as migrations and socioeconomic background. These distinctions are not just academic but have practical consequences. Owing to interaction with the environment, genetic predispositions to depression should not be viewed as unmodifiable destiny. Patients may genetically differ not just in their response to drugs, as in the now well-recognised field of pharmacogenetics, but also in how they react to stressful environments and how they are affected by behavioural therapies.
压力是抑郁症最重要的直接促发因素,但大多数大规模全基因组关联研究(GWAS)并未将压力作为一个变量纳入。在此,我们回顾基因×环境(G×E)相互作用可能如何阻碍遗传因素的发现,讨论抑郁症和成瘾领域中G×E相互作用的两个例子、纳入高压力环境的研究以及即将开展的全基因组环境相互作用研究(GWEIS)浪潮。我们讨论了最近的研究,这些研究表明遗传分布会受到移民和社会经济背景等社会因素的影响。这些差异不仅具有学术意义,还具有实际影响。由于与环境的相互作用,抑郁症的遗传易感性不应被视为不可改变的命运。患者不仅在对药物的反应上可能存在基因差异,就像现在广为人知的药物遗传学领域那样,而且在对压力环境的反应方式以及行为疗法对他们的影响方式上也可能存在基因差异。