Lack of genetic association of cholesteryl ester transfer protein polymorphisms with late onset Alzheimers disease.
Title | Lack of genetic association of cholesteryl ester transfer protein polymorphisms with late onset Alzheimers disease. |
Publication Type | Journal Article |
Year of Publication | 2005 |
Authors | Zhu, H, Gopalraj, RK, Kelly, JF, Bennett, DA, Estus, S |
Journal | Neurosci Lett |
Volume | 381 |
Issue | 1-2 |
Pagination | 36-41 |
Date Published | 2005 Jun 10-17 |
ISSN | 0304-3940 |
Keywords | Aged, Aged, 80 and over, Alzheimer Disease, Carrier Proteins, Cholesterol Ester Transfer Proteins, Cohort Studies, DNA Mutational Analysis, Female, Genetic Predisposition to Disease, Genetic Testing, Glycoproteins, Humans, Incidence, Kentucky, Male, Polymorphism, Genetic, Risk Assessment, Risk Factors, Statistics as Topic |
Abstract | Dysregulation of cholesterol homeostasis may be associated with the pathogenesis of coronary artery disease (CAD) and Alzheimers disease (AD). Recently, several single nucleotide polymorphisms (SNPs) in cholesteryl ester transfer protein (CETP) were associated with altered plasma CETP concentrations, cholesterol concentrations and CAD. Hence, these CETP SNPs represent excellent candidates for evaluating association with AD. To date, one study has evaluated the association between a single CETP SNP and AD. In this study, we examined three CETP SNPs to evaluate the genetic association of CETP with late onset AD on two study cohorts: the Religious Orders Study (ROS) series, including 85 AD and 70 non-AD individuals, and the University of Kentucky (UKY) series, including 78 AD and 84 non-AD individuals. Significant association between CETP genotypes or haplotypes and late onset AD was not detected in these two study cohorts. Moreover, the CETP genotypes and haplotypes were not significantly associated with AD when the populations were stratified for the presence or absence of apolipoprotein E4 (apoE4). In summary, CETP genetic variants were not associated with AD in two series. |
DOI | 10.1016/j.neulet.2005.01.078 |
Alternate Journal | Neurosci. Lett. |
PubMed ID | 15882786 |
Grant List | 2P50AG05144 / AG / NIA NIH HHS / United States P30AG10161 / AG / NIA NIH HHS / United States R01AG15819 / AG / NIA NIH HHS / United States R01AG2136 / AG / NIA NIH HHS / United States R01AG21545 / AG / NIA NIH HHS / United States |