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Stroke. 2007;38:2356-2359
Published online before print June 28, 2007, doi: 10.1161/STROKEAHA.107.482661
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(Stroke. 2007;38:2356.)
© 2007 American Heart Association, Inc.


Research Letters

CRP Gene Haplotypes, Serum CRP, and Cerebral Small-Vessel Disease

The Rotterdam Scan Study and the MEMO Study

Christiane Reitz, MD, PhD; Klaus Berger, MD, MPH; Moniek P.M. de Maat, PhD; Monika Stoll, PhD; Frauke Friedrichs, PhD; Isabella Kardys, MD; Jacqueline C.M. Witteman, PhD Monique M.B. Breteler, MD, PhD

From the Institute of Epidemiology and Social Medicine (C.R., K.B.) and the Leibniz Institute for Arteriosclerosis Research (M.S., F.F.), Genetic Epidemiology of Vascular Disorders, University of Muenster, Muenster, Germany, and the Departments of Hematology (M.P.M.d.M.) and of Epidemiology and Biostatistics (C.R., I.K., J.C.M.W., M.M.B.B.), Erasmus Medical Center, Rotterdam, The Netherlands.

Correspondence to M.M.B. Breteler, Department of Epidemiology & Biostatistics, Erasmus Medical Center, PO Box 1738, 3000DR Rotterdam, The Netherlands. Phone: +31 10 408 7489, fax: +31 10 408 9382. E-mail m.breteler{at}erasmusmc.nl

Abstract

Background and Purpose— It remains unclear whether C-reactive protein (CRP) is a serum marker for atherothrombotic disease or a causal factor in the pathogenesis of atherosclerosis. We explored the association between CRP gene variations and cerebral small-vessel disease (SVD) in the Rotterdam Scan Study (N=1035) and the MEMO Study (N=268).

Methods— Common haplotypes within the CRP gene were determined by genotype-tagging single-nucleotide polymorphisms. Then their relation with periventricular and subcortical white matter lesions and the prevalence of lacunar brain infarcts was explored by regression analyses.

Results— There was no association between CRP haplotypes and measures of cerebral SVD in either study. There was no effect modification of the association between serum CRP levels and measures of SVD by CRP haplotypes.

Conclusions— Our observations suggest that CRP is not causally involved in the pathogenesis of SVD.


Key Words: genetics • inflammation • lacunar infarcts • white matter disease




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