Journal
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
Volume 49, Issue 10, Pages 1020-1030Publisher
WILEY
DOI: 10.1111/j.1469-7610.2008.01909.x
Keywords
Epigenetics; DNA methylation; environment; prenatal; attention-deficit hyperactivity disorder (ADHD); genetics; psychiatry; DOHaD; fetal programming
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Funding
- Canadian Institutes of Health Research (CIHR) Postdoctoral Fellowship
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Attention-deficit hyperactivity disorder (ADHD) is a common childhood neurobehavioural disorder defined by symptoms of developmentally inappropriate inattention, impulsivity and hyperactivity. As is the norm for most psychiatric phenotypes, traditional aetiological studies have focused primarily on the interplay between genetic and environmental factors. It is likely that epigenetic factors, i.e., heritable, but reversible changes to genomic function that are independent of DNA sequence, are also important. It is known that epigenetic processes can be induced following exposure to a range of external factors, and thus provide a mechanism by which the environment can lead to long-term alterations in phenotype. In this article we hypothesise that epigenetic dysregulation may mediate the association observed between early-development environmental insults and ADHD. We propose that understanding the epigenetic processes involved in linking specific environmental pathogens to an increased risk for ADHD may offer new possibilities for preventative and therapeutic intervention.
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