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

Am J Med Genet. 2002 Apr 8;114(3):269-71. doi: 10.1002/ajmg.10253.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Attention Deficit Disorder with Hyperactivity / genetics*
  • Case-Control Studies
  • Gene Frequency
  • Humans
  • Membrane Proteins / genetics*
  • Microsatellite Repeats / genetics*
  • Nerve Tissue Proteins / genetics*
  • Polymorphism, Genetic
  • Synaptosomal-Associated Protein 25


  • Membrane Proteins
  • Nerve Tissue Proteins
  • SNAP25 protein, human
  • Synaptosomal-Associated Protein 25