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NEUROLOGY 2004;63:173-175
© 2004 American Academy of Neurology
Brief Communications

Possible association of nicastrin polymorphisms and Alzheimer disease in the Finnish population

S. Helisalmi, PhD, B. Dermaut, MD PhD, M. Hiltunen, PhD, A. Mannermaa, PhD, M. Van den Broeck, M. Lehtovirta, MD PhD, A. M. Koivisto, MD, S. Iivonen, MSc, M. Cruts, PhD, H. Soininen, MD PhD and C. Van Broeckhoven, PhD DSc

From the Departments of Neuroscience and Neurology (Drs. Helisalmi, Hiltunen, Lehtovirta, Koivisto, Iivonen, and Soininen) and Pathology (Dr. Mannermaa), Kuopio University Hospital and University of Kuopio, Finland; and Department of Molecular Genetics (Drs. Helisalmi, Dermaut, Van den Broeck, Cruts, and Van Broeckhoven), Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Antwerpen, Belgium.

Address correspondence and reprint requests to Dr. C. Van Broeckhoven, Department of Molecular Genetics VIB8, University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium; e-mail: christine.vanbroeckhoven{at}ua.ac.be

The authors previously reported that genetic variation in the gene coding for nicastrin (NCSTN) modified risk for familial early-onset Alzheimer disease (AD) in a Dutch population-based sample. Risk was highest in patients without an APOE {epsilon}4 allele. Here, they evaluated if NCSTN polymorphisms increased risk of AD in the eastern Finnish population. A significant difference in one haplotype was observed in AD patients without the APOE {epsilon}4 allele.

Received November 3, 2003. Accepted in final form February 27, 2004.






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