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.
|Number of pages||3|
|Journal||American Journal of Medical Genetics Part B: Neuropsychiatric Genetics|
|Early online date||18 Mar 2002|
|Publication status||Published - 8 Apr 2002|
- attention deficit hyperactivity disorder (ADHD)
- association study