Neurobiology of Lipids Noteworthy Articles

Noteworthy section of the Neurobiology of Lipids (ISSN 1683-5506) alerts interested readers about the selected noteworthy original research and viewpoint/review articles, book reviews, and meeting reports (published in other journals) on the subject of the journal scope

NoL Home | Noteworthy home | NoL Content | Archiving your research in NoL is a new service by the Neurobiology of Lipids NoL archives your research | Mission | PubMed | IFORA | Affiliates  | Contact us
For Graduate students: Assistant Editor and Research Assistant Opportunities

December 26, 2007

No association of genetic variants of liver X receptor-beta with Alzheimer's disease risk

Write to authors to ask them to make this article freely available at NoL Archive

Am J Med Genet B Neuropsychiatr Genet. 2007 Dec 14 [Epub ahead of print]
Rodriguez-Rodriguez E, Llorca J, Mateo I, Infante J, Sanchez-Quintana C, Garcia-Gorostiaga I, Fernandez-Viadero C, Pena N, Berciano J, Combarros O.
Neurology Service and Centro de Investigacion Biomedica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), "Marques de Valdecilla" University Hospital (University of Cantabria), Santander, Spain.

Apolipoprotein E (APOE) epsilon4 allele is the strongest hitherto known risk factor for sporadic Alzheimer's disease (AD). Liver X receptor-beta (LXRbeta) is a transcription factor that controls expression of genes involved in brain cholesterol metabolism, and one of the main LXRbeta targets is APOE. To evaluate the relationship between LXRbeta genetic variants and AD, independently or in concert with the APOE epsilon4 allele, we examined three LXRbeta polymorphisms located in introns 2 (rs 2695121), 5 (rs 1052533), and 7 (rs 1405655), in 414 Spanish AD patients and 447 controls. The current study does not demonstrate an association between LXRbeta genotypes or haplotypes and AD, neither in the total sample nor when the populations were stratified for the presence or absence of the APOE epsilon4 allele.

PubMed ID and Record

0 Comments:

Post a Comment

<< Home