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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). 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. Results: 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. |