Hawi, Ziarih; Kent, L.; Hill, M.; Anney, Richard J.L.; Brookes, Keeley J.; Barry, B.; Franke, Barbara; Banaschewski, Tobias; Buitelaar, Jan K.; Ebstein, Richard; Miranda, Ana; Oades, Robert D.; Roeyers, Herbert; Rothenberger, Aribert; Sergeant, Joseph A.; Gill, Michael et al:
ADHD and DAT1: further evidence of paternal over transmission of risk alleles and haplotype.
In: American Journal of Medical Genetics, Part B : Neuropsychiatric Genetics, Jg. 153 (2010), Heft 1, S. 97 - 102
2010Artikel/Aufsatz in ZeitschriftOA Grün
MedizinMedizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie, Psychosomatik und Psychotherapie des Kindes- und Jugendalters
Damit verbunden: 1 Publikation(en)
Titel in Englisch:
ADHD and DAT1: further evidence of paternal over transmission of risk alleles and haplotype.
Autor*in:
Hawi, Ziarih;Kent, L.;Hill, M.;Anney, Richard J.L.;Brookes, Keeley J.;Barry, B.;Franke, Barbara;Banaschewski, Tobias;Buitelaar, Jan K.;Ebstein, Richard;Miranda, Ana;Oades, Robert D.UDE
GND
1208788639
LSF ID
29685
ORCID
0000-0001-6151-5559ORCID iD
Sonstiges
der Hochschule zugeordnete*r Autor*in
;
Roeyers, Herbert;Rothenberger, Aribert;Sergeant, Joseph A.;Sonuga-Barke, Edmund J.S.;Steinhausen, Hans-Christian;Faraone, Stephen V.;Asherson, Philip;Gill, Michael
Erscheinungsjahr:
2010
Open Access?:
OA Grün
DuEPublico 1 ID
EVALuna Biblio ID
16392
Web of Science ID
PubMed ID
Sprache des Textes:
Englisch

Abstract:

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 3′-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 over-transmission 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.