No association between polymorphisms in the lectin-like oxidised low density lipoprotein receptor (ORL1) gene on chromosome 12 and Alzheimer's disease in a UK cohort

Antonia Pritchard, D St Clair, H Lemmon, DMA Mann, Corinne Lendon

    Research output: Contribution to journalArticle

    12 Citations (Scopus)

    Abstract

    Genome scans in sporadic Alzheimer's disease (AD) have revealed possible susceptibility loci on chromosome 12. Recently, two studies were published investigating the +1071 and +1073 polymorphisms in the lectin-like oxidised low density lipoprotein receptor (OLR1) gene with AD, a gene that lies within the area of chromosome 12 linkage. OLR1 is a good candidate gene, due to its function in lipid metabolism pathways, other components of which have been previously implicated as risk factors for AD. We undertook an association study in our UK cohort of 356 AD patients and 358 matched controls, using the same polymorphisms and performing the same sub-group and haplotype analysis as previously described. We found no association with AD in our case-control group as a whole, or when stratified into those with early (65 years) onset. When the group was split into APOE 4 bearers and 4 non-bearers, we could not confirm the associations described in the original study. Similarly, no significant differences were observed between AD patients and controls, in terms of their haplotype distributions. Therefore, in this present study, we find no evidence for the involvement of these ORL1 polymorphisms in increasing susceptibility to AD.
    Original languageEnglish
    Pages (from-to)126-129
    Number of pages4
    JournalNeuroscience Letters
    Volume366
    Issue number2
    DOIs
    Publication statusPublished - 1 Jan 2004

    Keywords

    • chromosome 12
    • OLR1
    • Alzheimer's
    • association study

    Fingerprint

    Dive into the research topics of 'No association between polymorphisms in the lectin-like oxidised low density lipoprotein receptor (ORL1) gene on chromosome 12 and Alzheimer's disease in a UK cohort'. Together they form a unique fingerprint.

    Cite this