Final published version
Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - Quantitative trait locus analysis of candidate gene alleles associated with attention deficit hyperactivity disorder (ADHD) in five genes
T2 - DRD4, DAT1, DRD5, SNAP-25, and 5HT1B
AU - Mill, Jonathan
AU - Xu, Xiaohui
AU - Ronald, Angelica
AU - Curran, Sarah
AU - Price, Tom
AU - Knight, Jo
AU - Craig, Ian
AU - Sham, Pak
AU - Plomin, Robert
AU - Asherson, Philip
N1 - (c) 2004 Wiley-Liss, Inc.
PY - 2005/2/5
Y1 - 2005/2/5
N2 - It has been widely postulated that the categorical diagnosis of attention deficit hyperactivity disorder (ADHD) should be seen as the extreme end of a set of traits quantitatively distributed in the general population. A consequence of this is that the genes associated with DSM-IV ADHD should also influence these underlying traits in non-affected individuals. The aim of this study was to examine if specific candidate loci previously shown to be associated with DSM-IV ADHD, also act as quantitative trait loci (QTLs) for ADHD-symptoms in the general population. We have genotyped five candidate markers in a population-based sample of male dizygous twin-pairs (n = 329 pairs). We found little evidence to support a role for the previously-nominated alleles of a DRD4 VNTR, a 5HT1B SNP, or a microsatellite marker near to DRD5, in the distribution of ADHD-symptoms scores; however, we found some evidence to suggest that the DAT1 3'UTR VNTR and weak evidence that a microsatellite in SNAP-25 may have a role in continuous measures of ADHD-symptoms hyperactivity above and beyond their role in clinical ADHD.
AB - It has been widely postulated that the categorical diagnosis of attention deficit hyperactivity disorder (ADHD) should be seen as the extreme end of a set of traits quantitatively distributed in the general population. A consequence of this is that the genes associated with DSM-IV ADHD should also influence these underlying traits in non-affected individuals. The aim of this study was to examine if specific candidate loci previously shown to be associated with DSM-IV ADHD, also act as quantitative trait loci (QTLs) for ADHD-symptoms in the general population. We have genotyped five candidate markers in a population-based sample of male dizygous twin-pairs (n = 329 pairs). We found little evidence to support a role for the previously-nominated alleles of a DRD4 VNTR, a 5HT1B SNP, or a microsatellite marker near to DRD5, in the distribution of ADHD-symptoms scores; however, we found some evidence to suggest that the DAT1 3'UTR VNTR and weak evidence that a microsatellite in SNAP-25 may have a role in continuous measures of ADHD-symptoms hyperactivity above and beyond their role in clinical ADHD.
KW - Alleles
KW - Attention Deficit Disorder with Hyperactivity
KW - Child
KW - Dopamine Plasma Membrane Transport Proteins
KW - Gene Frequency
KW - Genetic Predisposition to Disease
KW - Genotype
KW - Humans
KW - Linkage Disequilibrium
KW - Male
KW - Membrane Glycoproteins
KW - Membrane Proteins
KW - Membrane Transport Proteins
KW - Meta-Analysis as Topic
KW - Nerve Tissue Proteins
KW - Polymorphism, Genetic
KW - Quantitative Trait Loci
KW - Receptor, Serotonin, 5-HT1B
KW - Receptors, Dopamine D1
KW - Receptors, Dopamine D2
KW - Receptors, Dopamine D4
KW - Receptors, Dopamine D5
KW - Synaptosomal-Associated Protein 25
KW - Twins, Dizygotic
U2 - 10.1002/ajmg.b.30107
DO - 10.1002/ajmg.b.30107
M3 - Journal article
C2 - 15578613
VL - 133B
SP - 68
EP - 73
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 -