Association Study of a SNAP-25 Microsatellite and Attention Deficit Hpyeractivity Disorder

J Mill; S Curran; Lindsey Kent; A Gould; X Huckett; S Richards; E Taylor; P Asherson

doi:10.1002/ajmg.10253

Association Study of a SNAP-25 Microsatellite and Attention Deficit Hpyeractivity Disorder

J Mill, S Curran, Lindsey Kent, A Gould, X Huckett, S Richards, E Taylor, P Asherson

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85 Citations (Scopus)

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. (C) 2002 Wiley-Liss, Inc.

Original language	English
Pages (from-to)	269-271
Number of pages	3
Journal	American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume	114
Issue number	3
Early online date	18 Mar 2002
DOIs	https://doi.org/10.1002/ajmg.10253
Publication status	Published - 8 Apr 2002

Keywords

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

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10.1002/ajmg.10253

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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. (C) 2002 Wiley-Liss, Inc.",

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AU - Mill, J

AU - Curran, S

AU - Kent, Lindsey

AU - Gould, A

AU - Huckett, X

AU - Richards, S

AU - Taylor, E

AU - Asherson, P

PY - 2002/4/8

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N2 - 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.

AB - 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.

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Association Study of a SNAP-25 Microsatellite and Attention Deficit Hpyeractivity Disorder

Abstract

Keywords

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