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Iron is a reactive oxygen species and has been implicated in the pathogenesis of Alzheimer's disease (AD). In a population-based cohort study, including 268 incident AD patients and 2079 control individuals, we investigated the influence of the HFE C282Y and H63D variants and the apolipoprotein E4 (APOE epsilon 4) allele on the incidence, and age at onset of AD. There was no significant difference in the frequency of HFE variants in AD patients compared to controls. There was no significant effect modification by the APOE epsilon 4 allele. The mean age at onset was earlier in H63D homozygotes compared to non-carriers of this variant, in men (76.9+/-3.2 compared to 82.2+/-1.7) and women (82.1+/-3.9 compared to 84.5+/-1.7). In addition, in APOE epsilon 4 carriers, the mean age at onset of AD was earlier in men homozygous for the H63D variant (73.2+/-2.1 versus 78.7+/-1.6, p=0.05). Our results suggest that HFE variants are not strong determinants of AD in the general population but may modify the age of onset.

Original publication

DOI

10.1016/j.neurobiolaging.2007.05.026

Type

Journal article

Journal

Neurobiology of aging

Publication Date

02/2009

Volume

30

Pages

330 - 332

Addresses

Department of Epidemiology & Biostatistics, Erasmus Medical Centre Rotterdam, Rotterdam, The Netherlands.

Keywords

Humans, Alzheimer Disease, Genetic Predisposition to Disease, Apolipoproteins E, Membrane Proteins, Histocompatibility Antigens Class I, Incidence, Risk Assessment, Risk Factors, Age of Onset, Age Distribution, Polymorphism, Single Nucleotide, Aged, Aged, 80 and over, Middle Aged, Netherlands, Female, Male, Genetic Variation, Hemochromatosis Protein