JAMA Neurology ( IF 20.4 ) Pub Date : 2020-01-01 , DOI: 10.1001/jamaneurol.2019.3419 Sara Bandres-Ciga 1, 2 , Alastair J Noyce 3, 4 , Bryan J Traynor 5, 6
In 1986, Katan1 described a novel method to reliably estimate the effects of a causal variable without the need to conduct a traditional controlled trial.2 Now known as mendelian randomization (MR), this approach relies on the random assortment of genes (and noncoding DNA) as described by Mendel’s second law of inheritance. At the kernel of MR is the notion that this shuffling of DNA evenly distributes confounding factors, and this pattern, which remains unaltered through the lifetime of an individual, can be used to simulate the effect of modifiable factors (exposures) on susceptibility to a disease (outcome).3
中文翻译:
孟德尔随机化-从模糊到中间阶段的旅程,途中有几个坑洞。
1986年,Katan 1描述了一种新颖的方法,可以可靠地估计因果变量的影响,而无需进行传统的对照试验。2现在称为孟德尔随机化(MR),此方法依赖于孟德尔第二遗传定律所描述的基因(和非编码DNA)的随机分类。MR的核心思想是这种DNA改组均匀分布了混杂因素,并且这种模式在个体的一生中都没有改变,可以用来模拟可修饰因素(暴露)对疾病易感性的影响(结果)。3