No association between low density lipoprotein receptor genetic variants and Alzheimer's disease risk
✍ Scribed by Eloy Rodríguez; Ignacio Mateo; Javier Llorca; Coro Sánchez-Quintana; Jon Infante; José Berciano; Onofre Combarros
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 59 KB
- Volume
- 141B
- Category
- Article
- ISSN
- 1552-4841
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
A number of studies suggest that brain cholesterol metabolism may play a role in Alzheimer's disease (AD) development, probably through modulation of amyloid beta production. The discovery that apolipoprotein E (APOE) ε4 allele is a risk factor for sporadic AD raises the possibility that the receptors to which APOE binds on the surface of neurons are also involved in the neurodegenerative process. To evaluate the relationship between low density lipoprotein receptor (LDLR) genetic variant and AD, independently or in concert with the APOE ε4 allele, we examined three LDLR polymorphisms located in exons 8 (rs 11669576), 10 (rs 5930), and 13 (rs 5925), in a large group of 322 Spanish AD patients and 314 controls. The current study does not demonstrate an association between LDLR genotypes or haplotypes and AD, neither in the total sample nor when the populations were stratified for the presence or absence of the APOE ε4 allele. © 2006 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
The -4 allele of apolipoprotein E (APOE) is associated with increased risk of Alzheimer's disease (AD), but the pathogenic mechanism is unknown. The 5-repeat allele of a CGG repeat polymorphism in the 5 untranslated region of the very low-density lipoprotein receptor (VLDL-R) gene, a receptor for ap
atrophy (SMA) type I1 and 111 in the same sibship are not caused by different alleles at the SMA locus on 5q. Am J Hum