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

Nature Neuroscience volume 15, pages 181189 (2012) | Download Citation

Abstract

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.

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Acknowledgements

This work was supported in part by US National Institutes of Health grants DA18673 (M.C.N., H.M.), AA011408, AA017828, DA030005 (K.S.K., B.R.), AA018755, AA15416 (D.D.), DA023549 (N.G.), DA025109, DA022989, DA024413, DA027070, MH084952 (H.M.) and DA019498 (X.C.).

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Affiliations

  1. Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia and Virginia Commonwealth University, Richmond, Virginia, USA.

    • Kenneth S Kendler
    • , Xiangning Chen
    • , Danielle Dick
    • , Hermine Maes
    • , Nathan Gillespie
    • , Michael C Neale
    •  & Brien Riley
  2. Department of Psychiatry, Medical College of Virginia and Virginia Commonwealth University, Richmond, Virginia, USA.

    • Kenneth S Kendler
    • , Xiangning Chen
    • , Danielle Dick
    • , Hermine Maes
    • , Nathan Gillespie
    • , Michael C Neale
    •  & Brien Riley
  3. Department of Human and Molecular Genetics, Medical College of Virginia and Virginia Commonwealth University, Richmond, Virginia, USA.

    • Kenneth S Kendler
    • , Xiangning Chen
    • , Hermine Maes
    • , Michael C Neale
    •  & Brien Riley

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The authors declare no competing financial interests.

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Correspondence to Kenneth S Kendler.

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https://doi.org/10.1038/nn.3018

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