Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD

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Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD. / Mill, J.; Richards, S.; Knight, Jo et al.
In: Molecular Psychiatry, Vol. 9, No. 8, 08.2004, p. 801-810.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Mill, J, Richards, S, Knight, J, Curran, S, Taylor, E & Asherson, P 2004, 'Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD', Molecular Psychiatry, vol. 9, no. 8, pp. 801-810. https://doi.org/10.1038/sj.mp.4001482

APA

Mill, J., Richards, S., Knight, J., Curran, S., Taylor, E., & Asherson, P. (2004). Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD. Molecular Psychiatry, 9(8), 801-810. https://doi.org/10.1038/sj.mp.4001482

Vancouver

Mill J, Richards S, Knight J, Curran S, Taylor E, Asherson P. Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD. Molecular Psychiatry. 2004 Aug;9(8):801-810. Epub 2004 Mar 9. doi: 10.1038/sj.mp.4001482

Author

Mill, J. ; Richards, S. ; Knight, Jo et al. / Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD. In: Molecular Psychiatry. 2004 ; Vol. 9, No. 8. pp. 801-810.

Bibtex

@article{c5fd558dabeb4766bfbfcb74bd61315c,

title = "Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD",

abstract = "Several lines of evidence suggest a role for SNAP-25 (synaptosomal-associated protein of 25 kDa) in the genetic aetiology of ADHD. Most notable is the coloboma mouse mutant, which displays spontaneous hyperactivity and is hemizygous for a deletion spanning this gene. We have screened the SNAP-25 gene using denaturing high-performance liquid chromatography and sequencing, and genotyped six polymorphic single-nucleotide polymorphisms and two microsatellites in a clinically ascertained sample of 188 probands. Several markers were found to show association with ADHD, both individually and in combination with other markers to form multimarker haplotypes. Analyses of transmission by parental sex suggested that the association of SNAP-25 with ADHD is largely due to transmission of alleles from paternal chromosomes to affected probands, suggesting that this locus may be subject to genomic imprinting. Overall our data provide some evidence for a role of this gene in ADHD, although the precise causal functional variant is yet to be ascertained.",

keywords = "Attention Deficit Disorder with Hyperactivity, Base Sequence, DNA Primers, Exons, Family, Female, Genetic Markers, Genotype, Haplotypes, Humans, Male, Membrane Proteins, Nerve Tissue Proteins, Polymorphism, Genetic, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, Synaptosomal-Associated Protein 25",

author = "J. Mill and S. Richards and Jo Knight and S. Curran and Eleanor Taylor and Philip Asherson",

year = "2004",

month = aug,

doi = "10.1038/sj.mp.4001482",

language = "English",

volume = "9",

pages = "801--810",

journal = "Molecular Psychiatry",

issn = "1359-4184",

publisher = "Nature Publishing Group",

number = "8",

}

RIS

TY - JOUR

T1 - Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD

AU - Mill, J.

AU - Richards, S.

AU - Knight, Jo

AU - Curran, S.

AU - Taylor, Eleanor

AU - Asherson, Philip

PY - 2004/8

Y1 - 2004/8

N2 - Several lines of evidence suggest a role for SNAP-25 (synaptosomal-associated protein of 25 kDa) in the genetic aetiology of ADHD. Most notable is the coloboma mouse mutant, which displays spontaneous hyperactivity and is hemizygous for a deletion spanning this gene. We have screened the SNAP-25 gene using denaturing high-performance liquid chromatography and sequencing, and genotyped six polymorphic single-nucleotide polymorphisms and two microsatellites in a clinically ascertained sample of 188 probands. Several markers were found to show association with ADHD, both individually and in combination with other markers to form multimarker haplotypes. Analyses of transmission by parental sex suggested that the association of SNAP-25 with ADHD is largely due to transmission of alleles from paternal chromosomes to affected probands, suggesting that this locus may be subject to genomic imprinting. Overall our data provide some evidence for a role of this gene in ADHD, although the precise causal functional variant is yet to be ascertained.

AB - Several lines of evidence suggest a role for SNAP-25 (synaptosomal-associated protein of 25 kDa) in the genetic aetiology of ADHD. Most notable is the coloboma mouse mutant, which displays spontaneous hyperactivity and is hemizygous for a deletion spanning this gene. We have screened the SNAP-25 gene using denaturing high-performance liquid chromatography and sequencing, and genotyped six polymorphic single-nucleotide polymorphisms and two microsatellites in a clinically ascertained sample of 188 probands. Several markers were found to show association with ADHD, both individually and in combination with other markers to form multimarker haplotypes. Analyses of transmission by parental sex suggested that the association of SNAP-25 with ADHD is largely due to transmission of alleles from paternal chromosomes to affected probands, suggesting that this locus may be subject to genomic imprinting. Overall our data provide some evidence for a role of this gene in ADHD, although the precise causal functional variant is yet to be ascertained.

KW - Attention Deficit Disorder with Hyperactivity

KW - Base Sequence

KW - DNA Primers

KW - Exons

KW - Family

KW - Female

KW - Genetic Markers

KW - Genotype

KW - Haplotypes

KW - Humans

KW - Male

KW - Membrane Proteins

KW - Nerve Tissue Proteins

KW - Polymorphism, Genetic

KW - Polymorphism, Single Nucleotide

KW - Promoter Regions, Genetic

KW - Synaptosomal-Associated Protein 25

U2 - 10.1038/sj.mp.4001482

DO - 10.1038/sj.mp.4001482

M3 - Journal article

C2 - 15007392

VL - 9

SP - 801

EP - 810

JO - Molecular Psychiatry

JF - Molecular Psychiatry

SN - 1359-4184

IS - 8

ER -

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