Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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

Neurobiol Aging

Publication Date

02/2009

Volume

30

Pages

330 - 332

Keywords

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