TY - JOUR
T1 - Epigenetics and ADHD
T2 - Reflections on Current Knowledge, Research Priorities and Translational Potential
AU - Cecil, Charlotte A.M.
AU - Nigg, Joel T.
N1 - Funding Information:
Charlotte Cecil has received funding for this work from the European Union’s Horizon 2020 Research and Innovation Programme (EarlyCause; grant agreement no. 848158) and the European Research Council (TEMPO; grant agreement no. 101039672). Joel Nigg has received funding for this work from the National Institutes of Health (grant no. MH-R3759104). The views in this paper do not necessarily represent the views of the National Institutes of Health, the European Research Council, or the Horizon Programme.
Publisher Copyright:
© 2022, The Author(s).
PY - 2022/11
Y1 - 2022/11
N2 - Attention-deficit/hyperactivity disorder (ADHD) is a common and debilitating neurodevelopmental disorder influenced by both genetic and environmental factors, typically identified in the school-age years but hypothesized to have developmental origins beginning in utero. To improve current strategies for prediction, prevention and treatment, a central challenge is to delineate how, at a molecular level, genetic and environmental influences jointly shape ADHD risk, phenotypic presentation, and developmental course. Epigenetic processes that regulate gene expression, such as DNA methylation, have emerged as a promising molecular system in the search for both biomarkers and mechanisms to address this challenge. In this Current Opinion, we discuss the relevance of epigenetics (specifically DNA methylation) for ADHD research and clinical practice, starting with the current state of knowledge, what challenges we have yet to overcome, and what the future may hold in terms of methylation-based applications for personalized medicine in ADHD. We conclude that the field of epigenetics and ADHD is promising but is still in its infancy, and the potential for transformative translational applications remains a distant goal. Nevertheless, rapid methodological advances, together with the rise of collaborative science and increased availability of high-quality, longitudinal data make this a thriving research area that in future may contribute to the development of new tools for improved prediction, management, and treatment of ADHD.
AB - Attention-deficit/hyperactivity disorder (ADHD) is a common and debilitating neurodevelopmental disorder influenced by both genetic and environmental factors, typically identified in the school-age years but hypothesized to have developmental origins beginning in utero. To improve current strategies for prediction, prevention and treatment, a central challenge is to delineate how, at a molecular level, genetic and environmental influences jointly shape ADHD risk, phenotypic presentation, and developmental course. Epigenetic processes that regulate gene expression, such as DNA methylation, have emerged as a promising molecular system in the search for both biomarkers and mechanisms to address this challenge. In this Current Opinion, we discuss the relevance of epigenetics (specifically DNA methylation) for ADHD research and clinical practice, starting with the current state of knowledge, what challenges we have yet to overcome, and what the future may hold in terms of methylation-based applications for personalized medicine in ADHD. We conclude that the field of epigenetics and ADHD is promising but is still in its infancy, and the potential for transformative translational applications remains a distant goal. Nevertheless, rapid methodological advances, together with the rise of collaborative science and increased availability of high-quality, longitudinal data make this a thriving research area that in future may contribute to the development of new tools for improved prediction, management, and treatment of ADHD.
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U2 - 10.1007/s40291-022-00609-y
DO - 10.1007/s40291-022-00609-y
M3 - Article
C2 - 35933504
AN - SCOPUS:85135521717
SN - 1177-1062
VL - 26
SP - 581
EP - 606
JO - Molecular Diagnosis and Therapy
JF - Molecular Diagnosis and Therapy
IS - 6
ER -