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From the Department of Neurodegenerative Diseases (R.F.-S., M.S., J.C.M. C.K., T.G.), Hertie-Institute for Clinical Brain Research, Eberhard-Karls University, Tuebingen, Germany; Graduate School of Cellular and Molecular Neurosciences (R.F.-S.), International Max Plank Research School, Eberhard-Karls University, Tuebingen, Germany; Institute for Medical Statistics and Epidemiology and Institute for Psychiatry and Psychotherapy (J.C.M.), Technical University Munich, Germany; Institute for Epidemiology (H.G., T.I.), GSF-National Research Centre for Environment and Health, Neuherberg, Germany; Department of Neurology (J.A.), Grosshadern University Hospital, Ludwig-Maximilians University, Munich, Germany; Department of Neurology (C.M., A.L.), University Hospital of Ulm, Ulm, Germany.
Address correspondence and reprint requests to Dr. Thomas Gasser, Department of Neurodegenerative Diseases, Hertie-Institute for Brain Research, Hoppe-Seyler Str. 3, Tuebingen, Germany 72076; e-mail: thomas.gasser{at}med.uni-tuebingen.de.
Individuals homozygous for haplotypes -2578-A/-1154-A/-634-G or -2578-A/-1154-G/-634-G in the promoter/5'UTR of the VEGF gene have a 1.8-fold increased risk of ALS in several European populations. We did not observe any significant association with single markers, or haplotype pairs, in a German sample of 580 sporadic ALS patients and 628 controls. However, the promoter SNP-1154 (rs1570360) was associated with affection status in women (p = 0.036), suggesting that the VEGF effect may be dependent on the sex ratio of the sample.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the June 27 issue to find the title link for this article.
Disclosure: The authors report no conflicts of interest.
Received July 19, 2005. Accepted in final form February 28, 2006.
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