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Psychiatr Genet DOI:10.1097/YPG.0b013e32834c0cc8

Sex-specific influence of DRD2 on ADHD-type temperament in a large population-based birth cohort.

Publication TypeJournal Article
Year of Publication2012
AuthorsNyman, ES, Loukola, A, Varilo, T, Taanila, A, Hurtig, T, Moilanen, I, Loo, S, McGough, JJ, Jarvelin, M-R, Smalley, SL, Nelson, SF, Peltonen, L
JournalPsychiatr Genet
Date Published2012 Aug
KeywordsAttention Deficit Disorder with Hyperactivity, Cohort Studies, Female, Finland, Gene Frequency, Genetic Predisposition to Disease, Genetics, Population, Humans, Male, Parturition, Receptors, Dopamine D2, Sex Characteristics, Temperament

Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder with a significant public-health impact. Previously, we described a candidate gene study in a population-based birth cohort that demonstrated an association with ADHD-affected males and the dopamine receptor D2 (DRD2). The current study evaluates potential associations of dopamine receptor genes and Cloninger temperament traits within this same sample. Participants with stringent lifetime ADHD diagnoses were ascertained systematically from the genetically isolated Northern Finland 1986 Birth Cohort (n=9432), resulting in 178 cases and 157 controls. Markers in all known dopamine receptor genes were genotyped. We report an association of DRD2 with low Persistence in females (rs1079727 P=0.02, rs1124491 P=0.02, rs1800497 P=0.03). The associated DRD2 minor allelic haplotype (CAA, P=0.03) is the same haplotype we previously associated with ADHD in males in this birth cohort. The current study further supports previous results on the role of DRD2 in individuals with ADHD. Investigations suggest that DRD2 may have an impact on both males and females, but the particular outcome appears sex-specific, manifesting as ADHD in males and low Persistence in females. Furthermore, these findings suggest that the putative role of low Persistence as an endophenotype for ADHD deserves further investigation.


Alternate JournalPsychiatr. Genet.
PubMed ID22531292
Grant ListMH01966 / MH / NIMH NIH HHS / United States
MH063706 / MH / NIMH NIH HHS / United States