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A genomewide scan for loci involved in attention-deficit/hyperactivity disorder.

Simon E. Fisher,¹ Clyde Francks,¹ James T. McCracken,² James J. McGough,² Angela J. Marlow,1 I. Laurence MacPhie,1 Dianne F. Newbury,1 Lori R. Crawford,2 Christina G. S. Palmer,² J. Arthur Woodward,³ Melissa Del’Homme,² Dennis P. Cantwell,^* Stanley F. Nelson,² Anthony P. Monaco,¹ and Susan L. Smalley^2
1Wellcome Trust Centre for Human Genetics, Oxford University, Oxford; and ²UCLA Center for Neurobehavioral
Wellcome Trust Centre for Human Genetics, Oxford University, Oxford, United Kingdom.

The Wellcome Trust Centre for Human Genetics (WTCHG) was established in 1994 to undertake research into the genetic basis of common diseases. Since June 2000 the Centre has been located in the Henry Wellcome Building of Genomic Medicine, University of Oxford.

The scientific objective of the Centre is to explore all aspects of the genetic susceptibility of disease including the localisation of genes involved in common diseases, characterisation of the variants responsible for susceptibility, the understanding of how these DNA variants may contribute to risk of disease in the population and finally, how such genetic factors contribute biologically to a disease process.

The Centre houses multi-disciplinary research teams in human genetics, functional genomics, bioinformatics, statistical genetics and structural biology.

A genomewide scan for loci involved in attention-deficit/hyperactivity disorder.

Attention deficit/hyperactivity disorder (ADHD) is a common heritable disorder with a childhood onset. Molecular genetic studies of ADHD have previously focused on examining the roles of specific candidate genes, primarily those involved in dopaminergic pathways. We have performed the first systematic genomewide linkage scan for loci influencing ADHD in 126 affected sib pairs, using a approximately 10-cM grid of microsatellite markers. Allele-sharing linkage methods enabled us to exclude any loci with a lambda(s) of > or =3 from 96% of the genome and those with a lambda(s) of > or =2.5 from 91%, indicating that there is unlikely to be a major gene involved in ADHD susceptibility in our sample. Under a strict diagnostic scheme we could exclude all screened regions of the X chromosome for a locus-specific lambda(s) of >/=2 in brother-brother pairs, demonstrating that the excess of affected males with ADHD is probably not attributable to a major X-linked effect. Qualitative trait maximum LOD score analyses pointed to a number of chromosomal sites that may contain genetic risk factors of moderate effect. None exceeded genomewide significance thresholds, but LOD scores were >1.5 for regions on 5p12, 10q26, 12q23, and 16p13. Quantitative-trait analysis of ADHD symptom counts implicated a region on 12p13 (maximum LOD 2.6) that also yielded a LOD >1 when qualitative methods were used. A survey of regions containing 36 genes that have been proposed as candidates for ADHD indicated that 29 of these genes, including DRD4 and DAT1, could be excluded for a lambda(s) of 2. Only three of the candidates-DRD5, 5HTT, and CALCYON-coincided with sites of positive linkage identified by our screen. Two of the regions highlighted in the present study, 2q24 and 16p13, coincided with the top linkage peaks reported by a recent genome-scan study of autistic sib pairs.

Taken from ADHD Research, for more details on this research:
well.ox.ac.uk
Which has been created and maintained by Dr. Simon Fisher

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