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Arch Neurol. 1998;55:1053-1054.

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

FIVE YEARS ago, Saunders et al¹ reported the strong and surprising association between apolipoprotein E (apoE) genotypes and sporadic Alzheimer disease (AD). There are 3 common alleles of the apoE gene: 2, 3, and 4 , with allele frequencies in the general population of approximately 0.08, 0.78, and 0.14, respectively. There is universal agreement that the 4 allele is a powerful risk factor for AD that lowers the age of dementia onset, whereas the 2 allele may protect against AD or at least delay its onset. During the past 5 years, research on apoE and AD has centered on 3 broad questions: (1) Do apoE genotypes influence the phenotype of AD? (2) Can the apoE genotype be used to diagnose AD? (3) What are the biological mechanisms whereby the 4 allele increases the risk of developing AD? The study by Jonker et al² touches on each . . . [Full Text of this Article]

DO apoE GENOTYPES INFLUENCE THE PHENOTYPE OF AD?


CAN THE apoE GENOTYPE BE USED IN THE DIAGNOSIS OF AD?

WHAT ARE THE BIOLOGICAL MECHANISMS WHEREBY THE 4 ALLELE INCREASES THE RISK OF DEVELOPING AD?

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