TY - JOUR
T1 - Parent of origin effects in attention/deficit hyperactivity disorder (ADHD)
T2 - Analysis of data from the international multicenter ADHD genetics (IMAGE) program
AU - Anney, Richard J.L.
AU - Hawi, Ziarih
AU - Sheehan, Karen
AU - Mulligan, Aisling
AU - Pinto, Carlos
AU - Brookes, Keeley J.
AU - Xu, Xiaohui
AU - Zhou, Kaixin
AU - Franke, Barbara
AU - Buitelaar, Jan
AU - Vermeulen, Sita H.
AU - Banaschewski, Tobias
AU - Sonuga-Barke, Edmund
AU - Ebstein, Richard
AU - Manor, Iris
AU - Miranda, Ana
AU - Mulas, Fernando
AU - Oades, Robert D.
AU - Roeyers, Herbert
AU - Rommelse, Nanda
AU - Rothenberger, Aribert
AU - Sergeant, Joseph
AU - Steinhausen, Hans Christoph
AU - Taylor, Eric
AU - Thompson, Margaret
AU - Asherson, Philip
AU - Faraone, Stephen V.
AU - Gill, Michael
PY - 2008/12/5
Y1 - 2008/12/5
N2 - There are conflicting reports suggesting that the parental origin of transmitted risk alleles may play a role in the etiology of attention deficit/hyperactivity disorder (ADHD). A recent report by Hawi and colleagues observed a generalized paternal over-transmission of alleles associated with ADHD. This was not replicated in more recent studies. Using data from a large multicenter study we examined the overall and gene-specific parent of origin effect in 554 independent SNPs across 47 genes. Transmission disequilibrium and explicit parent of origin test were performed using PLINK. Overall parent of origin effect was tested by Chi-square. There was no overall parent of origin effect in the IMAGE sample (χ12 = 1:82, P = 0.117). Five markers in three genes, DDC, TPH2, and SLC6A2 showed nominal association (P < 0.01) with ADHD combined subtype when restricted to maternal or paternal transmission only. Following the initial report by Hawi and co-workers three studies, including this one, found 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 etiology ADHD.
AB - There are conflicting reports suggesting that the parental origin of transmitted risk alleles may play a role in the etiology of attention deficit/hyperactivity disorder (ADHD). A recent report by Hawi and colleagues observed a generalized paternal over-transmission of alleles associated with ADHD. This was not replicated in more recent studies. Using data from a large multicenter study we examined the overall and gene-specific parent of origin effect in 554 independent SNPs across 47 genes. Transmission disequilibrium and explicit parent of origin test were performed using PLINK. Overall parent of origin effect was tested by Chi-square. There was no overall parent of origin effect in the IMAGE sample (χ12 = 1:82, P = 0.117). Five markers in three genes, DDC, TPH2, and SLC6A2 showed nominal association (P < 0.01) with ADHD combined subtype when restricted to maternal or paternal transmission only. Following the initial report by Hawi and co-workers three studies, including this one, found 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 etiology ADHD.
KW - ADHD
KW - Candidate gene
KW - Parent of origin effect
UR - http://www.scopus.com/inward/record.url?scp=57349170939&partnerID=8YFLogxK
U2 - 10.1002/ajmg.b.30659
DO - 10.1002/ajmg.b.30659
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C2 - 18163388
AN - SCOPUS:57349170939
SN - 1552-4841
VL - 147
SP - 1495
EP - 1500
JO - American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
JF - American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
IS - 8
ER -