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An association study of the cholesteryl ester transfer protein TaqI B polymorphism with late onset Alzheimer's disease.

TitleAn association study of the cholesteryl ester transfer protein TaqI B polymorphism with late onset Alzheimer's disease.
Publication TypeJournal Article
Year of Publication2004
AuthorsFidani, L., Goulas A., Crook R., Petersen R. C., Tangalos E., Kotsis A., & Hardy J.
JournalNeurosci Lett
Volume357
Issue2
Pagination152-4
Date Published2004 Mar 04
ISSN0304-3940
KeywordsAged, Aged, 80 and over, Alzheimer Disease, Carrier Proteins, Chi-Square Distribution, Cholesterol Ester Transfer Proteins, Deoxyribonucleases, Type II Site-Specific, Female, Gene Frequency, Glycoproteins, Humans, Logistic Models, Male, Odds Ratio, Polymorphism, Genetic
Abstract

Cholesteryl ester transfer protein (CETP) is reportedly able to affect the amount of cholesterol available for deposition and/or removal from peripheral tissues, in its capacity to mediate the transfer of cholesterol from high density lipoprotein (HDL) to very low density lipoprotein, in exchange for triacylglycerols from the latter. The TaqI B polymorphism of the human CETP gene has been associated with decreased CETP mass and an increase in HDL-cholesterol. While many studies have addressed the atherogenic or anti-atherogenic potential of this polymorphism, little is known about its effect on neurodegeneration, despite the fact that CETP is expressed in the brain and the disturbance of cholesterol homeostasis appears to be an important factor in the pathogenesis of Alzheimer's disease (AD). In this report, we have compared the distribution of the TaqI B polymorphism in an independent population of 102 clinically diagnosed late onset AD patients and a spousal control group of 97 individuals. We have also examined the possible interaction between this polymorphism and two other polymorphisms suspected of affecting cholesterol flux, namely apolipoprotein E APOE epsilon4, and lipoprotein lipase LPLS447X. No statistically significant differences have emerged with respect to either genotype or allele frequencies between the AD and control populations. CETP TaqI B did not interact significantly with either APOE epsilon4 or LPLS447X, in this study.

DOI10.1016/j.neulet.2003.11.071
Alternate JournalNeurosci Lett
PubMed ID15036597
Grant ListAG 06786 / AG / NIA NIH HHS / United States
AG 16574 / AG / NIA NIH HHS / United States
AG 21013 / AG / NIA NIH HHS / United States

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