TY - JOUR
T1 - ADHD and DAT1: Further evidence of paternal over-transmission of risk alleles and haplotype
AU - Hawi, Z.
AU - Kent, L.
AU - Hill, M.
AU - Anney, R.J.
AU - Brookes, K. J.
AU - Barry, E.
AU - Franke, B.
AU - Banaschewski, T.
AU - Buitelaar, J.
AU - Ebstein, R.
AU - Miranda, A.
AU - Oades, R.D.
AU - Roeyers, H.
AU - Rothenberger, A.
AU - Sergeant, J.A.
AU - Sonuga-Barke, E.
AU - Steinhausen, H.C.
AU - Faraone, S.V.
AU - Asherson, P.
AU - Gill, M.
PY - 2009
Y1 - 2009
N2 - We [Hawi et al. (2005); Am J Hum Genet 77:958-965] reported paternal over-transmission of risk alleles in some ADHD-associated genes. This was particularly clear in the case of the DAT1 30-UTR VNTR. In the current investigation, we analyzed three new sample comprising of 1,248 ADHD nuclear families to examine the allelic over-transmission of DAT1 in ADHD. The IMAGE sample, the largest of the three-replication samples, provides strong support for a parent of origin effect for allele 6 and the 10 repeat allele (intron 8 and 3′-UTR VNTR, respectively) of DAT1. In addition, a similar pattern of overtransmission of paternal risk haplotypes (constructed from the above alleles) was also observed. Some support is also derived from the two smaller samples although neither is independently significant. Although the mechanism driving the paternal over-transmission of the DAT risk alleles is not known, these finding provide further support for this phenomenon. © 2009 Wiley-Liss, Inc.
AB - We [Hawi et al. (2005); Am J Hum Genet 77:958-965] reported paternal over-transmission of risk alleles in some ADHD-associated genes. This was particularly clear in the case of the DAT1 30-UTR VNTR. In the current investigation, we analyzed three new sample comprising of 1,248 ADHD nuclear families to examine the allelic over-transmission of DAT1 in ADHD. The IMAGE sample, the largest of the three-replication samples, provides strong support for a parent of origin effect for allele 6 and the 10 repeat allele (intron 8 and 3′-UTR VNTR, respectively) of DAT1. In addition, a similar pattern of overtransmission of paternal risk haplotypes (constructed from the above alleles) was also observed. Some support is also derived from the two smaller samples although neither is independently significant. Although the mechanism driving the paternal over-transmission of the DAT risk alleles is not known, these finding provide further support for this phenomenon. © 2009 Wiley-Liss, Inc.
U2 - 10.1002/ajmg.b.30960
DO - 10.1002/ajmg.b.30960
M3 - Article
SN - 1552-4841
VL - 153B
SP - 97
EP - 102
JO - American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
JF - American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
IS - 1
ER -
