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From the Davee Department of Neurology and Clinical Neurosciences (W.C., M.S., H.M., N.S., L.D., W.-Y.H., H.-X.D., R.L.S., S.L.H., T.S.), Feinberg School of Medicine, Northwestern University, Chicago, IL; Center for Human Genetics Research (J.L.H.), Vanderbilt University Medical Center, Nashville, TN; Center for Human Genetics (M.P.-V.), Duke University Medical Center, Durham, NC; Department of Cell and Molecular Biology (T.S.); Northwestern University Institute of Neuroscience, Chicago, IL.
Address correspondence and reprint requests to Dr. Teepu Siddique, Davee Department of Neurology and Clinical Neurosciences and Department of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Tarry Building, Room 13-715, 303 East Chicago Avenue, Chicago, IL 60611; e-mail: t-siddique{at}northwestern.edu
The authors tested the association of three vascular endothelial growth factor (VEGF) promoter polymorphisms with sporadic ALS (SALS) to verify the results of a previous study and to investigate their modifier effects on the subphenotypes of SALS in a large family-based and case-control cohort of North American white subjects (N = 1,603). They did not find any association of the VEGF promoter polymorphisms with SALS or its subphenotypes, suggesting that they do not have a direct causal role in ALS.
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 August 8 issue to find the title link for this article.
*These authors contributed equally to this work.
Supported by National Institute of Neurologic Disorders and Stroke (NS050641, NS046535), Les Turner ALS Foundation, V.E. Schaff ALS Research Fund, H. Post Research Professorship, Wenske Foundation, Falk Medical Research Trust, Abbott Labs Duane and Susan Burnham Professorship, and the David C. Asselin, MD, Memorial Fund.
Disclosure: The authors report no conflicts of interest.
Received January 23, 2006. Accepted in final form March 31, 2006.
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