Association study of a SNAP‐25 microsatellite and attention deficit hyperactivity disorder |
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Authors: | Sarah Curran Lindsey Kent Alison Gould Louise Huckett Sandra Richards Eric Taylor Philip Asherson |
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Affiliation: | 1. Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London, United Kingdom;2. Department of Psychiatry, University of Birmingham, Edgbaston, Birmingham, United Kingdom |
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Abstract: | 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. © 2002 Wiley‐Liss, Inc. |
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Keywords: | attention deficit hyperactivity disorder (ADHD) SNAP‐25 genetics association study
bA416N4
HS1068F16
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