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No association between CCL2 gene polymorphisms and risk of inflammatory demyelinating diseases in a Korean population

Authors

  • S. Namgoong,

    1. Department of Life Science, Sogang University, Seoul, Republic of Korea
    2. Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea
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    • These authors contributed equally to this work.
  • J. S. Bae,

    1. Laboratory of Translational Genomics, Samsung Genome Institute, Samsung Medical Center, Seoul, Republic of Korea
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    • These authors contributed equally to this work.
  • H. S. Cheong,

    1. Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea
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  • J.-H. Kim,

    1. Research Institute for Basic Science, Sogang University, Seoul, Republic of Korea
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  • J. Y. Kim,

    1. Department of Life Science, Sogang University, Seoul, Republic of Korea
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  • L. H. Kim,

    1. Department of Life Science, Sogang University, Seoul, Republic of Korea
    2. Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea
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  • H. J. Kim,

    1. Department of Neurology, National Cancer Center, Gyeonggi-do, Republic of Korea
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  • H. D. Shin

    Corresponding author
    1. Department of Life Science, Sogang University, Seoul, Republic of Korea
    2. Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea
    3. Research Institute for Basic Science, Sogang University, Seoul, Republic of Korea
    • Correspondence

      Dr Hyoung Doo Shin

      Department of Life Science

      Sogang University

      35 Baekbeom-ro

      Mapo-gu

      Seoul 121-742

      Republic of Korea

      Tel: +82 2 3273 1671

      Fax: +82 2 3273 1680

      e-mail: hdshin@sogang.ac.kr

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Abstract

Inflammatory demyelinating disease (IDD), which includes multiple sclerosis (MS) and neuromyelitis optica (NMO), affects the central nervous system. Chemokine ligand 2 (CCL2/MCP-1) is considered an important contributor to the development or progression of IDD. However, genetic association studies of Asian populations are lacking. In this study, we investigated a possible association between CCL2 polymorphisms (rs1024611, rs28730833, and rs2857657) and a Korean population (178 IDD patients and 237 healthy controls) using multiple logistic regression models. However, we did not find any association, which was consistent with other studies in Caucasian populations. In conclusion, our results suggest that CCL2 variants may not contribute to the pathogenesis of IDD.

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