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Prevalence of haemochromatosis gene mutations in Parkinson’s disease
  1. Anne Hege Aamodt1,
  2. Lars Jacob Stovner1,
  3. Ketil Thorstensen3,
  4. Stian Lydersen4,
  5. Linda R White1,
  6. Jan O Aasly2
  1. 1Department of Neuroscience, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
  2. 2Department of Neurology, St Olav’s Hospital, Trondheim, Norway
  3. 3Department of Medical Biochemistry, St Olav’s Hospital, Trondheim, Norway
  4. 4Unit for Applied Clinical Research, Norwegian University of Science and Technology, Trondheim, Norway
  1. Correspondence to:
 Dr Anne Hege Aamodt
 Department of Neurology, St Olav’s Hospital, N-7006 Trondheim, Norway; anne.hege.aamodt{at}ntnu.no

Abstract

The aim of this study was to investigate a possible association between haemochromatosis (HFE) gene mutations and the prevalence of Parkinson’s disease. The HFE gene encodes a protein that modulates iron absorption. Several studies have documented increased iron levels in the basal ganglia in patients with Parkinson’s disease. In a study on patients with concurrent hereditary haemochromatosis and Parkinson’s disease, abnormal deposition of iron in the basal ganglia was suggested as an inductor of Parkinson’s disease. In this study, genotype frequencies of the HFE mutations C282Y, H63D and S65C were estimated in 388 patients with Parkinson’s disease and compared with frequencies found in comparable studies. No significant differences were found in frequencies between the patients and comparable populations. This study does not indicate increased susceptibility to Parkinson’s disease in HFE gene mutation carriers in Norway.

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Footnotes

  • Competing interests: None.

  • Published Online First 20 October 2006

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