Abstract

AbstractAlthough there is an impressive literature documenting both a strong participation of genetics in the etiology of attention‐deficit/hyperactivity disorder (ADHD) and a high rate of response to stimulants and atomoxetine, surprisingly few studies on the pharmacogenomics of ADHD were conducted. This review aims to present a critical discussion of findings from recent investigations on this emerging new area of research. We performed a systematic computer review of the literature on ADHD pharmacogenomics. In addition, we contacted some research centers involved in research on ADHD genetics, asking for any kind of nonpublished data relevant for the topic of this revision. This review strategy identified only seven papers presenting nonduplicated research findings on ADHD pharmacogenomics. Contact with other investigators resulted in five more studies presented in medical meetings or still nonpublished. The majority of investigations are on dopaminergic genes, especially on polymorphisms at the dopamine transporter gene (DAT1). Although there were some instigating preliminary results suggesting the association between the homozygosity for the 10‐repeat allele at DAT1 gene and response to methylphenidate, recent studies were not able to replicate these previous findings. Very few investigations addressed the role of nondopaminergic genes, or gene‐to‐gene interactions in ADHD pharmacogenomics. Pharmacogenomic studies of ADHD are in their infancy. We presented a discussion on the limitations and possible future directions of the research in the field. Drug Dev. Res. 62:172–179, 2004. © 2004 Wiley‐Liss, Inc.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.