Published Online
on June 28, 2007

A more recent version of this article appeared on August 1, 2007

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Submitted on January 17, 2007
Accepted on February 13, 2007

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; and 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.

^* To whom correspondence should be addressed. E-mail: m.breteler{at}erasmusmc.nl.

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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