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Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder

dc.contributor.authorZhou, K.
dc.contributor.authorDempfle, A.
dc.contributor.authorArcos-Burgos, Mauricio
dc.contributor.authorBakker, S. C.
dc.contributor.authorBanaschewski, T.
dc.contributor.authorBiederman, J.
dc.contributor.authorBuitelaar, J.
dc.contributor.authorCastellanos, F. X.
dc.contributor.authorDoyle, A.
dc.contributor.authorEbstein, R. P.
dc.date.accessioned2015-12-13T22:55:17Z
dc.date.issued2008
dc.date.updated2016-02-24T08:36:50Z
dc.description.abstractGenetic contribution to the development of attention deficit hyperactivity disorder (ADHD) is well established. Seven independent genome-wide linkage scans have been performed to map loci that increase the risk for ADHD. Although significant linkage signals were identified in some of the studies, there has been limited replications between the various independent datasets. The current study gathered the results from all seven of the ADHD linkage scans and performed a Genome Scan Meta Analysis (GSMA) to identify the genomic region with most consistent linkage evidence across the studies. Genome-wide significant linkage (PSR = 0.00034, POR = 0.04) was identified on chromosome 16 between 64 and 83 Mb. In addition there are nine other genomic regions from the GSMA showing nominal or suggestive evidence of linkage. All these linkage results may be informative and focus the search for novel ADHD susceptibility genes.
dc.identifier.issn1552-4841
dc.identifier.urihttp://hdl.handle.net/1885/82464
dc.publisherJohn Wiley & Sons Inc
dc.sourceAmerican Journal of Medical Genetics, Part B: Neuropsychiatric
dc.subjectKeywords: article; attention deficit disorder; chromosome 16; genetic analysis; genetic linkage; genetic susceptibility; human; priority journal; Attention Deficit Disorder with Hyperactivity; Chromosome Mapping; Chromosomes, Human, Pair 16; European Continental An ADHD; GSMA; Linkage
dc.titleMeta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder
dc.typeJournal article
local.bibliographicCitation.issue8
local.bibliographicCitation.lastpage1398
local.bibliographicCitation.startpage1392
local.contributor.affiliationZhou, K., Kings College London
local.contributor.affiliationDempfle, A., Phillips-University Marburg
local.contributor.affiliationArcos-Burgos, Mauricio (Oscar), College of Medicine, Biology and Environment, ANU
local.contributor.affiliationBakker, S.C., University of Miami
local.contributor.affiliationBanaschewski, T, University of Heidelberg
local.contributor.affiliationBiederman, J., Massachusetts General Hospital
local.contributor.affiliationBuitelaar, J., Radboud University Nijmegen
local.contributor.affiliationCastellanos, F.X., New York University Child Study Center
local.contributor.affiliationDoyle, A., Harvard Medical School
local.contributor.affiliationEbstein, R.P., Geha MHC
local.contributor.authoruidArcos-Burgos, Mauricio (Oscar), u5088570
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.identifier.absfor060408 - Genomics
local.identifier.ariespublicationf5625xPUB10719
local.identifier.citationvolume147
local.identifier.doi10.1002/ajmg.b.30878
local.identifier.scopusID2-s2.0-57349131186
local.type.statusPublished Version

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