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Apolipoprotein E genotype and statins affect CRP levels through independent and different mechanisms: AGES-Reykjavik

Gudny Eiriksdottir, Thor Aspelund, Kristjana Bjarnadottir

    Atherosclerosis
    |February 1, 2006
    PubMed

    Insights

    The apolipoprotein E (APOE) epsilon4 allele is linked to lower C-reactive protein (CRP) levels, independent of statin use. This genetic effect on inflammation may occur through a distinct mechanism.

    Area of Science:

    • Genetics and Cardiovascular Health
    • Inflammation Biomarkers

    Background:

    • C-reactive protein (CRP) is an inflammatory marker associated with coronary heart disease (CHD).
    • The apolipoprotein E (APOE) epsilon4 allele has been linked to lower CRP levels.
    • Statin treatment also reduces CRP levels, complicating the interpretation of genetic associations.

    Purpose of the Study:

    • To investigate the association between APOE genotypes and CRP levels in the AGES-Reykjavik Study.
    • To account for the influence of statin treatment, prior CHD, and erythrocyte sedimentation rate (ESR) on this association.

    Main Methods:

    • Genotyping of APOE alleles in 2296 participants from the AGES-Reykjavik Study.
    • Measurement of high-sensitivity C-reactive protein (hs-CRP) levels.
    • Analysis using a general linear model to assess the relationship between APOE genotype and CRP.

    Main Results:

    • APOE epsilon4 allele carriers exhibited significantly lower CRP levels compared to non-carriers.
    • This reduction in CRP was dose-dependent, with individuals carrying two epsilon4 alleles showing the lowest levels.
    • The association between APOE epsilon4 and lower CRP persisted regardless of statin use.

    Conclusions:

    • The epsilon4 allele independently contributes to lower CRP levels.
    • This genetic effect on CRP appears to operate via a mechanism distinct from that of statin therapy.
    • Further research is warranted to elucidate the specific pathways involved.
    Abstract

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