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RESEARCH PRODUCT
ADHD and DAT1: Further evidence of paternal over-transmission of risk alleles and haplotype
Herbert RoeyersKeely Joanne BrookesLindsey KentHans-christoph SteinhausenHans-christoph SteinhausenHans-christoph SteinhausenStephen V. FaraoneRichard P. EbsteinMichael GillAna MirandaMatthew HillPhilip AshersonRichard AnneyJan K. BuitelaarRobert D. OadesJoseph A. SergeantZiarih HawiTobias BanaschewskiEdwina BarryEdmund J.s. Sonuga-barkeAribert RothenbergerBarbara Frankesubject
Untranslated region2716 Genetics (clinical)Candidate gene2804 Cellular and Molecular NeuroscienceMedizin610 Medicine & healthMinisatellite RepeatsBiology2738 Psychiatry and Mental HealthGenomic Imprinting03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineSDG 3 - Good Health and Well-beingmental disordersPerception and Action [DCN 1]HumansGenetics(clinical)ddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersRisk factorAllele3' Untranslated RegionsNuclear familyGeneAllelesGenetics (clinical)GeneticsMental Health [NCEBP 9]Dopamine Plasma Membrane Transport ProteinsHaplotypeIntron10058 Department of Child and Adolescent Psychiatry030227 psychiatryPsychiatry and Mental healthHaplotypesAttention Deficit Disorder with Hyperactivity/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being030217 neurology & neurosurgerydescription
Contains fulltext : 87259.pdf (Publisher’s version ) (Closed access) 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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2010-01-05 | American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |