Nicotinic acetylcholine receptor 7 subunit gene and attention deficit hyperactivity disorder

L. Kent, E Green, Michael F Fitzgerald, Z. Hawi, M Gill, A. Thapar, J. Holmes, P. Asherson, A. Gould, E. Taylor, T. Payton, N. Craddock

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Attention deficit hyperactivity disorder (ADHD) is a highly heritable, common psychiatric disorder of childhood which probably involves several genes. There are several lines of evidence which suggest that the nicotinic system may be functionally significant in ADHD: 1).Nicotine promotes the release of dopamine, as does methylphenidate, the most widely used drug treatment for ADHD, 2). Rats demonstrate changes in locomotor activity after nicotine exposure and prenatal nicotine exposure produces reduced numbers of striatal dopaminergic receptor binding sites, 3). Nicotine has been shown to improve attention in smokers, non-smokers and adults with ADHD and 4). ADHD is a significant risk factor for early initiation of cigarette smoking in children and maternal cigarette smoking appears to be a risk factor for ADHD. The neuronal nicotinic acetylcholine receptor ?7 subunit gene (CHRNA7) has been previously implicated in attentional disturbances in patients with schizophrenia and in many of their non-schizophrenic relatives. We have undertaken a family based candidate gene association study of 230 parent-proband trios. Probands were aged 6-12 years and met DSM-IV criteria for ADHD based on semistructured parental interview (CAPA). Children with known major medical or psychiatric conditions or mental retardation (IQ

Original languageEnglish
Pages (from-to)490
Number of pages1
JournalAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume96
Issue number4
Publication statusPublished - 7 Aug 2000
Externally publishedYes

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