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No association between DNA repair gene XRCC1 and amyotrophic lateral sclerosis

  • Fang Fang

      Affiliations

    • Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA
    • Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
    • Corresponding Author InformationCorresponding author at: P.O. Box 281, Karolinska Institutet, Stockholm 171 77, Sweden. Tel: +46 8 524 86131; fax: +46 8 31 49 75
    • ,
  • David M. Umbach

      Affiliations

    • Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA
    • ,
  • Zongli Xu

      Affiliations

    • Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA
    • ,
  • Weimin Ye

      Affiliations

    • Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
    • ,
  • Dale P. Sandler

      Affiliations

    • Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA
    • ,
  • Jack A. Taylor

      Affiliations

    • Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA
    • ,
  • Freya Kamel

      Affiliations

    • Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA

Received 14 May 2010; received in revised form 1 July 2010; accepted 5 July 2010. published online 18 August 2010.
Corrected Proof

Abstract 

Reduced DNA repair capacity may play a role in amyotrophic lateral sclerosis (ALS) etiology. We examined the association between ALS risk and single nucleotide polymorphisms (SNPs) in the gene x-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1) utilizing data from a case-control study and 2 genome-wide association studies (the study of Irish Amyotrophic Lateral Sclerosis and the National Institute of Neurological Disorders and Stroke (NINDS) genome-wide study in Amyotrophic Lateral Sclerosis and Neurologically Normal Controls). Our results did not show any differences in the frequency of XRCC1 gene polymorphisms between ALS patients and controls free of any neurological disease.

Keywords: Amyotrophic lateral sclerosis, DNA repair, XRCC1

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PII: S0197-4580(10)00311-8

doi:10.1016/j.neurobiolaging.2010.07.004

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