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Lack of independent associations of apolipoprotein E promoter and intron 1 polymorphisms with Alzheimer's disease.

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By Rebeck GW, Cheung BS, Growdon WB, Deng A, Akuthota • www.ProHealth.com • September 17, 1999


Several studies have demonstrated genetic associations between Alzheimer's disease (AD) and polymorphisms in the promoter/enhancer regions of the apolipoprotein E (APOE) gene. These studies raise the possibility that APOE transcription control may be involved in altered risks for AD.

We evaluated polymorphic sites in the intron-1 enhancer element (IE-1G/C) and in the APOE promoter (-219G/T). For the IE-1 polymorphism, we analyzed 433 individuals (183 AD and 250 controls), and found a strong linkage between the IE-1G allele and APOE-epsilon4. When we controlled for this linkage using log-linear model analysis, we found no independent association between the IE-1 polymorphism and AD. For the -219 polymorphism, we analyzed 475 individuals (168 AD cases, 234 controls, and 73 cases of cerebral amyloid angiopathy (CAA)).

We found strong linkages between the -219G allele and APOE-epsilon2 and between the -219 T allele and APOE-epsilon4. Controlling for these linkages, we found no independent association between the -219 polymorphism and AD or CAA. Thus, our studies do not support independent associations between AD and either the IE-1 or the -219 polymorphisms.

Source: Neurosci Lett 1999 Sep 17;272(3):155-8
PMID: 10505604, UI: 99433423

(Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA. rebeck@helix.mgh.harvard.edu)




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