Abstract：
:The epsilon4 allele of the apolipoprotein E gene (APOE) has repeatedly been associated with increased risk for Alzheimer's disease (AD). Bullido and colleagues recently identified a polymorphism in the promoter region of the APOE gene (-491A/T) and found that -491A homozygosity predicted AD independently of APOE epsilon4. Since the -491A/T polymorphism and the known APOE polymorphism must be in tight linkage disequilibrium, and the later polymorphism is know to be associated with the disease, we wished to determine to what extent this linkage disequilibrium explained the -491A/T polymorphism association with Alzheimer's disease. We genotyped a community-based control sample (n = 132) and a clinic-based Alzheimer's disease sample (n = 190) for the known APOE and -491A/T polymorphisms, and find that, while the -491A/T polymorphism confers some independent risk for AD, linkage disequilibrium between the known APOE and -491A/T polymorphic sites explains most of the -491A association. Furthermore, when considering the known APOE and -491A/T polymorphisms alone, APOE epsilon4 status is the best predictor of the disease.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Town T,Paris D,Fallin D,Duara R,Barker W,Gold M,Crawford F,Mullan Mdoi
10.1016/s0304-3940(98)00567-9subject
Has Abstractpub_date
1998-08-14 00:00:00pages
95-8issue
2eissn
0304-3940issn
1872-7972pii
S0304394098005679journal_volume
252pub_type
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