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  Vol. 52 No. 7, July 1995 TABLE OF CONTENTS
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There Is a Pathologic Relationship Between ApoE-{varepsilon}4 and Alzheimer's Disease

Elizabeth H. Corder, PhD, MPH
Center for Demographic Studies Duke University Durham, NC 27708-0408

Ann M. Saunders, PhD; Margaret A. Pericak-Vance, PhD; Allen D. Roses, MD
Durham, NC

Arch Neurol. 1995;52(7):650.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The recently published letter by Riggs and Keefover1 suggests that the ever-present bane of epidemiologic studies, selection bias, may account for the "observed association between ApoE-{varepsilon}4 [apolipoprotein E {varepsilon}4 allele] and late-onset AD [Alzheimer's disease]." This association has now been replicated in many clinic-based epidemiologic and autopsy groups throughout the world.

We suspect that the delay in publication of the letter caused its authors to miss significant publications concerning the protective role of ApoE-{varepsilon}22-5 and the rationale for ApoE genotype—specific trajectories of risk for AD with increasing age (Figure). That risk related to the {varepsilon}4 allele and benefit related to the {varepsilon}2 allele diminish with age in surviving individuals is consistent with published work3,6 and work by others presented at scientific meetings.

The competing risks of heart disease and death also related to ApoE-{varepsilon}4 are unlikely to account for the ApoE-{varepsilon} . . . [Full Text PDF of this Article]



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