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NEUROLOGY 2005;65:934-937
© 2005 American Academy of Neurology


Brief Communications

Association of the H63D polymorphism in the hemochromatosis gene with sporadic ALS

E. F. Goodall, BSc, M. J. Greenway, MB, I. van Marion, BSc, C. B. Carroll, PhD, MRCP, O. Hardiman, MD, FRCPI and K. E. Morrison, DPhil, FRCP

From the Department of Clinical Neuroscience (E.F. Goodall, I. van Marion, Drs. Carroll, and Morrison), The Medical School, University of Birmingham, Birmingham, U.K.; Department of Clinical Neurological Sciences (Drs. Greenway and Hardiman), Royal College of Surgeons in Ireland, Dublin, Ireland; and Department of Neurology (Dr. Hardiman), Beaumont Hospital, Dublin, Ireland.

Address correspondence and reprint requests to Prof Morrison, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, U.K.; e-mail: k.morrison{at}bham.ac.uk

Iron misregulation promotes oxidative stress and abnormally high iron levels have been found in the spinal cords of patients with ALS. The authors investigated whether HFE gene polymorphisms, linked to hemochromatosis, are associated with ALS using two independent populations of patients with sporadic ALS and controls (totaling 379 patients and 400 controls). They found that the H63D polymorphism is overrepresented in individuals with sporadic ALS (odds ratio 1.85, CI: 1.35 to 2.54).


Funding from the Midlands Neuroscience Teaching and Research Fund, the University Hospital Birmingham Charities (I.V.M.) and the Medical Research Council (E.F.G.) is acknowledged.

Disclosure: The authors report no conflicts of interest.

Received March 4, 2005. Accepted in final form June 8, 2005.




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