LETTER TO JMG

No association between a previously reported OLR1 3' UTR polymorphism and Alzheimer’s disease in a large family sample

L Bertram¹, M Parkinson¹, K Mullin¹, R Menon¹, D Blacker^2,3, R E Tanzi¹

¹ Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease (MIND), Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
² Gerontology Research Unit, Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
³ Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA

Correspondence to:
Correspondence to:
R E Tanzi, PhD
Genetics and Aging Research Unit, MGH-East (MIND), 114 16^th St, Charlestown, MA 02129, USA; tanzi@helix.mgh.harvard.edu

Received 28 November 2003

Accepted 15 December 2003

Keywords: 2-macroglobulin; family-based association; linkage disequilibrium; oxidised LDL receptor 1

Abbreviations: A2M, 2-macroglobulin; AD, Alzheimer’s disease; APOE, apolipoprotein E; CLR, conditional logistic regression; EMSAs, electrophoretic mobility shift assays; LD, linkage disequilibrium; LRP1, low density lipoprotein-related protein 1; OLR1, oxidised LDL receptor 1

The first 150 words of the full text of this article appear below.

Recently, two studies^1,2 reported independent evidence of genetic association between a 3' UTR single nucleotide polymorphism (SNP; rs1050283, also known as "+1073") in the oxidised LDL receptor 1 gene (OLR1) on chromosome 12p13.2 and risk for Alzheimer’s disease (AD). The implied chromosomal area is a highly promising AD candidate region because both genetic linkage and association studies have reported significant signals to two different locations separated by about 40 Mb (about 44 cM): the more proximal region is located near 10 Mb, on 12p13, and contains OLR1 as well as the gene encoding 2-macroglobulin (A2M), while the more distal region near 50 Mb, on 12q13, maps close to the genes encoding LRP1 (low density lipoprotein-related protein 1) and TFCP2 (transcription factor CP2). All four of these genes have shown independent associations with AD risk, although the results for A2M and LRP1 have been controversial (for . . . [Full text of this article]

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