Haplotype analysis of the PARK 11 gene, GIGYF2, in sporadic Parkinson's disease

Authors

  • Greg T. Sutherland PhD,

    1. Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia
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  • Gerhard A. Siebert PhD,

    1. Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia
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  • Jeremy R. B. Newman BBiomedSc,

    1. Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia
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  • Peter A. Silburn PhD, FRACP,

    1. Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia
    2. UQ Centre for Clinical Research, School of Medicine, University of Queensland, Brisbane, Queensland Australia
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  • Richard S. Boyle FRACP,

    1. Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia
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  • John D. O'Sullivan FRACP,

    1. Department of Neurology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia
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  • George D. Mellick PhD

    Corresponding author
    1. Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Brisbane, Queensland, Australia
    2. Department of Neurology, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    3. Department of Neurology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia
    • Eskitis Institute for Cell and Molecular Therapies, School of Biomolecular and Physical Sciences, Griffith University, Nathan, Queensland 4111, Australia

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  • Potential conflict of interest: None reported.

Abstract

Familial Parkinsonism (PARK) genes are strong candidates for conferring susceptibility to common forms of PD. However, most studies to date have provided little evidence that their common variants substantially influence disease risk. Recently, mutations were described in the gene, GIGYF2 (TNRC15), located at the PARK11 locus (2q37.1). Here, we use a haplotype tagging approach to examine common variation in the GIGYF2 gene and PD risk. PD cases (n = 568) and age and gender-matched control subjects (n = 568) were recruited from three specialist movement disorder clinics in Brisbane (Australia) and the Australian electoral roll. Twelve tagging SNPs were assessed in all subjects and haplotype and genotype associations were explored. Overall our findings suggest that common genetic variants of GIGYF2 do not significantly affect sporadic PD risk in Australian Caucasians. © 2008 Movement Disorder Society

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