Abstract
A major risk determinant for late-onset Alzheimer’s disease (AD) is polymorphism in apolipoprotein E (ApoE), a protein which plays a critical role in redistributing cholesterol and other lipids to neurons. Of the three isoforms, ApoE4(R112,R158) is associated with an increased risk and ApoE2(C112,C158) is associated with a decreased risk of AD, relative to the common ApoE3(C112,R158) isoform. How single amino-acid changes can substantially alter AD pathology remains unclear, though several lines of evidence suggest that isoforms differ in lipid binding and subsequent binding to cell surfaces receptors.
Published Version
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