TY - JOUR
T1 - ADHD and DAT1: further evidence of paternal over-transmission of risk alleles and haplotype
AU - Hawi, Ziarih
AU - Kent, Lindsey S W
AU - Hill, Matthew James
AU - Anney, Richard J
AU - Brookes, Keely Joanne
AU - Barry, Edwina
AU - Franke, Barbara
AU - Banaschewski, Tobias
AU - Buitelaar, Jan K
AU - Ebstein, Richard P
AU - Miranda, Ana Lucia
AU - Oades, Robert D
AU - Roeyers, Herbert
AU - Rothenberger, Aribert
AU - Sergeant, Joseph A
AU - Sonuga-Barke, Edmund J S
AU - Steinhausen, Hans Christoph
AU - Faraone, Stephen V
AU - Asherson, Philip J
AU - Gill, Michael
PY - 2010
Y1 - 2010
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
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
UR - http://onlinelibrary.wiley.com/doi/10.1002/ajmg.b.30960/pdf
U2 - 10.1002/ajmg.b.30960
DO - 10.1002/ajmg.b.30960
M3 - Article
VL - 153
SP - 97
EP - 102
JO - American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
JF - American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
SN - 1552-4841
IS - 1
ER -