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British Medical Bulletin Advance Access originally published online on February 15, 2008
British Medical Bulletin 2008 85(1):35-45; doi:10.1093/bmb/ldn004
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Epigenetics: what is it and why is it important to mental disease?

Anthony R. Isles* and Lawrence S. Wilkinson

Behavioural Genetics Group, Department of Psychological Medicine, School of Medicine, and School of Psychology, Cardiff University, Cardiff, UK

* Correspondence to: Dr A. R. Isles, Behavioural Genetics Group, Department of Psychological Medicine, School of Medicine, and School of Psychology, 2nd Floor, Henry Wellcome Building, Heath Park, Cardiff CF14 4XN, UK. E-mail: IslesAR1{at}cardiff.ac.uk

Introduction: The chemical marking of the DNA and surrounding histone proteins represent some of the means by which gene expression is controlled. Many of these epigenetic modifications are pre-programmed and are an important part of the control of development.

Sources of data: There is an accumulating body of evidence from clinical genetics and animal work that suggests some epigenetic processes may also be labile.

Areas of agreement: A number of these studies have demonstrated that the epigenetic status of genes can be altered through environmental events such as in vitro culture of embryos and exposure to toxins, sometimes resulting in disease.

Areas of controversy: More routine variations in life events may also be encoded by changes in the epigenetic status of genes, and as such these processes may provide a mechanism mediating interplay between genes and the environment, including the now recognized idea of gene–environment interactions.

Growing points and areas timely for developing research: The significance of epigenetics for mental disease is becoming increasingly clear. It is important that the techniques developed to analyse the epigenome are now applied to the study of the molecular basis of mental disease to assess the contribution of gene–environment interactions to brain function.

Keywords: imprinted genes • gene expression • DNA methylation • histone modifications • Angelman • Prader–Willi • Rett • gene–environment interaction

Accepted for publication January 11, 2008.


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