Association study of DSM-IV attention deficit hyperactivity disorder (ADHD) and monoamine pathway genes

P Asherson, V Virdee, S Curran, L Ebersole, B Freeman, I Craig, E Simonoff, T Eley, R Plomin, E Taylor

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22 Citations (Scopus)


The regulation of dopamine and other monoamines has been implicated in both the aetiology of hyperactivity and the well-characterised response of hyperactivity to stimulants such as methylphendidate. More recently, deletion of Snap-25, DAT1, and DRD3 in mice has each been shown to cause markerd overactivity (responsive to amphetamine in the case of Snap-25). Studies in human samples with childhood ADHD suggest that genetic variation of DRD4 and DAT1 may both influence susceptibility to ADHD, although neither of these two associations are yet confirmed. We have collected a sample of 100 DSM-IV ADHD probands and matched controls. Association analysis of polymorphisms within DRD4, DAT1, DRD3, TH, SERT, NET1, and COMT, as well as mutation screening of Snap-25, has been performed. Data have been analysed in clinical groups of DSM-IV ADHD mixed type, categorised in several ways: (1) unselected for comorbid conditions or drug response, (2) no significant comorbid conditions, unselected for drug response (± conduct disorder), (3) no signficant comorbid disorders, methylphendidate responders only. To date, we have detected no significant associations with polymorphisms within these genes. In particular, our data do not lend support to the previously reported association with the 480 bp repeat allele of DAT1 [71%, 71%, 73%, and 73% in (1),(2),(3), and controls, respectively], or the reported association with the 7-repeat allele of DRD4 [13%, 12%, 11%, and 13% in (1), (2), (3), and controls, respectively].
Original languageEnglish
Pages (from-to)549-549
Number of pages1
JournalAmerican Journal of Medical Genetics
Issue number6
Early online date6 Nov 1998
Publication statusPublished - 6 Nov 1998


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