Association study of a SNAP-25 microsatellite and attention deficit hyperactivity disorder.

J Mill, S Curran, Lindsey Kent, Alison Gould, Louise Huckett, Sandra Richards, Eric Taylor, Philip Asherson

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85 Citations (Scopus)


Several lines of evidence implicate synaptosomal-associated protein of 25 kDa (SNAP-25) in the etiology of attention deficit hyperactivity disorder (ADHD). Most notably, the coloboma mouse mutant, considered to be a good animal model of hyperactivity, has a deletion spanning this gene. Introducing a SNAP-25 transgene into these animals alleviates hyperlocomotion. We have identified a novel microsatellite repeat in SNAP-25 located between the 5'UTR and the first coding exon, and tested for association with ADHD. Case-control analyses suggest there may be a role of this polymorphism in ADHD, with one allele over-represented in controls and another over-represented in probands. Within-family tests of linkage and association confirmed these findings. Further work is needed to ascertain the role of SNAP-25 in ADHD and assess the functional significance of this polymorphism. (C) 2002 Wiley-Liss, Inc.

Original languageEnglish
Pages (from-to)269-271
Number of pages3
JournalAmerican Journal of Medical Genetics
Publication statusPublished - 8 Apr 2002


  • attention deficit hyperactivity disorder (ADHD)
  • SNAP-25
  • genetics
  • association study
  • GENE


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