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Publication year
2008Author(s)
Source
American Journal of Medical Genetics. Part B : Neuropsychiatric Genetics, 147B, 8, (2008), pp. 1337-44ISSN
Publication type
Article / Letter to editor
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Organization
Human Genetics
Psychiatry
Health Evidence
Former Organization
Epidemiology, Biostatistics & HTA
Journal title
American Journal of Medical Genetics. Part B : Neuropsychiatric Genetics
Volume
vol. 147B
Issue
iss. 8
Page start
p. 1337
Page end
p. 44
Subject
DCN 1: Perception and Action; DCN 2: Functional Neurogenomics; DCN 3: Neuroinformatics; IGMD 3: Genomic disorders and inherited multi-system disorders; NCEBP 9: Mental health; NCMLS 6: Genetics and epigenetic pathways of disease; UMCN 3.2: Cognitive neurosciences; UMCN 5.1: Genetic defects of metabolismAbstract
Results of behavioral genetic and molecular genetic studies have converged to suggest that genes substantially contribute to the development of attention deficit/hyperactivity disorder (ADHD), a common disorder with an onset in childhood. Yet, despite numerous linkage and candidate gene studies, strongly consistent and replicable association has eluded detection. To search for ADHD susceptibility genes, we genotyped approximately 600,000 SNPs in 958 ADHD affected family trios. After cleaning the data, we analyzed 438,784 SNPs in 2,803 individuals comprising 909 complete trios using ADHD diagnosis as phenotype. We present the initial TDT findings as well as considerations for cleaning family-based TDT data. None of the SNP association tests achieved genome-wide significance, indicating that larger samples may be required to identify risk loci for ADHD. We additionally identify a systemic bias in family-based association, and suggest that variable missing genotype rates may be the source of this bias.
This item appears in the following Collection(s)
- Academic publications [248099]
- Electronic publications [135463]
- Faculty of Medical Sciences [94006]
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