Journal
AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
Volume 153B, Issue 4, Pages 955-959Publisher
WILEY
DOI: 10.1002/ajmg.b.31053
Keywords
transferrin; hemachromatosis gene; Alzheimer's disease; epistasis; genetic association
Categories
Funding
- National Institute on Aging (Washington University) [P50-AG05681, P01-AC03991, P01-AG026276, R01-AG16208, P30-N5057105, 1-TL1-RR024995-01, 1-KL2-RR024994-01]
- Barnes Jewish Foundation
- American Health Assistance Foundation
- National Center for Research Resources (NCRR) [UL1 RR024992]
- National Institutes of Health (NIH) [U01 AG024904]
- NIH Roadmap for Medical Research
- Hope Center for Neurological Disorders and National Institutes of Health [T32 MH14677]
- Fundacion Alfonso Martin Escudero
- National Institute of Biomedical Imaging and Bioengineering (NIBIB)
- MRC [G0300429] Funding Source: UKRI
- Medical Research Council [G0801418B, G0300429] Funding Source: researchfish
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Alzheimer's disease (AD) is a complex disease that is likely influenced by many genetic and environmental factors. Citing evidence that iron may play a role in All pathology, Robson et al. [Robson et al.(2004); J Med Genet 41:261-265] reported that epistatic interaction between rs1049296 (P589S) in the transferrin gene (TF) and rs1800562 (C282Y) in the hemochromatosis gene (HFE) results in significant association with risk for AD. In this study we attempted to replicate their findings in a total of 1,166 cases and 1,404 controls from three European and European American populations. Allele and genotype frequencies were consistent across the three populations. Using synergy factor analysis (SFA) and Logistic Regression analysis we tested each population and the combined sample for interactions between these two SNPs and risk for AD. We observed significant association between bi-carriers of the minor alleles of rs1049296 and rs1800562 in the combined sample using SFA (P=0.0016, synergy factor = 2.71) and adjusted SFA adjusting for age and presence of the APOE epsilon 4 allele (P=0.002, OR = 2.4). These results validate those of the previous report and support the hypothesis that iron transport and regulation play a role in AD pathology. (C) 2009 Wiley-Liss, Inc.
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