Anney, R. J. L., Hawi, Z., Sheehan, K., Mulligan, A., Lowe, N., Brookes, K., Franke, B., Buitelaar, J., Banaschewski, T., Sonuga-Barke, E. J. S., Ebstein, R., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Sergeant, J. A., Steinhausen, H-C., Taylor, E. A., Thompson, M., Asherson, P., Faraone, S. V., & Gill, M. (2008).
Parent of origin effects in attention-deficit/hyperactivity disorder (ADHD): analysis of data from the International Multicentre ADHD Genetics (IMAGE) programme.
American Journal of Medical Genetics, part B, 10.1002/ajmg.b.30659: (request a copy): view article

Introduction: There are conflicting reports suggesting that the parental origin of transmitted risk alleles may play a role in the aetiology of ADHD. A recent report by Hawi et al. observed a generalised paternal over-transmission of alleles associated with ADHD. -- This was not replicated in more recent studies.

Methods: Using data from a large multicentre study of ADHD we examined the overall & gene-specific parent of origin effect in 554 independent SNPs across 47 genes. Transmission disequilibrium & explicit parent of origin test were performed using PLINK. Overall parent of origin effect was tested by chi-square.


1/ There was no overall parent of origin effect in the IMAGE sample (×2 1=1.82, p=0.117).

2/ 5 markers in 3 genes, DDC (paternal: dopamine decarboxylase), TPH2 (serotonin synthesis) & SLC6A2 (noradrenaline transporter: NET) show nominal association (p<0.01) with ADHD combined subtype when restricted to maternal or paternal transmission only.

3/ In 3 follow-up studies, including data presented here, we find no evidence to support an overall parent of origin effect for markers associated with ADHD. We cannot however, exclude gene-specific parent of origin effect in the aetiology ADHD.

Support: NIH.