Recent advances in the genetic epidemiology and molecular genetics of substance use disorders

被引：111
作者：
Kendler, Kenneth S. [1 ,2 ,3 ]
Chen, Xiangning [1 ,2 ,3 ]
Dick, Danielle [1 ,2 ]
Maes, Hermine [1 ,2 ,3 ]
Gillespie, Nathan [1 ,2 ]
Neale, Michael C. [1 ,2 ,3 ]
Riley, Brien [1 ,2 ,3 ]
机构：
[1] Virginia Commonwealth Univ, Med Coll Virginia, Virginia Inst Psychiat & Behav Genet, Richmond, VA 23298 USA
[2] Virginia Commonwealth Univ, Med Coll Virginia, Dept Psychiat, Richmond, VA 23298 USA
[3] Virginia Commonwealth Univ, Med Coll Virginia, Dept Human & Mol Genet, Richmond, VA 23298 USA
来源：
NATURE NEUROSCIENCE | 2012年 / 15卷 / 02期
基金：
美国国家卫生研究院;
关键词：
ENVIRONMENTAL RISK-FACTORS; GENOME-WIDE ASSOCIATION; STRESSFUL LIFE EVENTS; LUNG-CANCER; NICOTINE DEPENDENCE; ALCOHOL DEPENDENCE; CHROMOSOME; 15Q25.1; SUSCEPTIBILITY LOCUS; CANNABIS INITIATION; DRUG-DEPENDENCE;
D O I：
10.1038/nn.3018
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
This article reviews current advances in the genetics of substance use disorders (SUDs). Both genetic and environmental sources of risk are required to develop a complete picture of SUD etiology. Genetic sources of risk for SUDs are not highly substance specific in their effects. Genetic and environmental risks for SUDs typically do not only add together but also interact with each other over development. Risk gene identification for SUDs has been difficult, with one recent success in identifying nicotinic receptor variants that affect risk for nicotine dependence. The impact of genetic variants on SUD risk will individually be small. Although genetic epidemiologic methods are giving us an increasingly accurate map of broad causal pathways to SUDs, gene discovery will be needed to identify the specific biological systems. Identifying these risk genes and understanding their action will require large clinical samples, and interaction between these studies and work in model organisms.
引用
收藏
页码：181 / 189
页数：9
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