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- Title
Association of the paternally transmitted copy of common Valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene with susceptibility to ADHD.
- Authors
Kent, L.; Green, E.; Hawi, Z.; Kirley, A.; Dudbridge, F.; Lowe, N.; Raybould, R.; Langley, K.; Bray, N.; Fitzgerald, M.; Owen, M. J.; O'Donovan, M. C.; Gill, M.; Thapar, A.; Craddock, N.
- Abstract
Attention deficit hyperactivity disorder (ADHD) is a common, highly heritable, neurodevelopmental disorder with onset in early childhood. Genes involved in neuronal development and growth are, thus, important etiological candidates and brain-derived neurotrophic factor (BDNF), has been hypothesized to play a role in the pathogenesis of ADHD. BDNF is a member of the neurotrophin family and is involved in the survival and differentiation of dopaminergic neurons in the developing brain (of relevance because drugs that block the dopamine transporter can be effective therapeutically). The common Val66Met functional polymorphism in the human BDNF gene (rs 6265) was genotyped in a collaborative family-based sample of 341 white UK or Irish ADHD probands and their parents. We found evidence for preferential transmission of the valine (G) allele of BDNF (odds ratio, OR=1.6, P=0.02) with a strong paternal effect (paternal transmissions: OR=3.2, P=0.0005; maternal transmissions: OR=1.00; P=1.00). Our findings support the hypothesis that BDNF is involved in the pathogenesis of ADHD. The transmission difference between parents raises the possibility that an epigenetic process may be involved.Molecular Psychiatry (2005) 10, 939–943. doi:10.1038/sj.mp.4001696; published online 31 May 2005
- Subjects
VALINE; BRANCHED chain amino acids; AMINO acids; ORGANIC acids; GENETIC polymorphisms; POPULATION genetics; NEUROTROPHINS; NEUROPHYSIOLOGY; ATTENTION-deficit hyperactivity disorder; BEHAVIOR disorders in children
- Publication
Molecular Psychiatry, 2005, Vol 10, Issue 10, p939
- ISSN
1359-4184
- Publication type
Article
- DOI
10.1038/sj.mp.4001696