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Despite biological support for a role of angiotensin converting enzyme (ACE) in Alzheimer's disease (AD), studies assessing the ACE I/D polymorphism in AD are conflicting. We re-evaluated this association in the Rotterdam Study, a population-based cohort study. The mechanism of association was further explored by adjusting for vascular factors, and by analysing atrophy, white matter lesions and infarcts on MRI in non-demented individuals. Genotypes were available for 6488 participants. During average follow-up of 6 years 250 subjects developed AD. MRI data were available for 494 non-demented participants. Homozygosity for the I-allele conferred a slightly increased risk of AD compared to carrying a D-allele (RR 1.12 (95% CI 0.99-1.25)). This increase was only significant in women, and independent of vascular factors (RR 1.39 (95% CI 1.14-1.69)). Non-demented women with the II genotype had smaller hippocampal and amygdalar volumes. Vascular pathology was not significantly associated with ACE. This suggests a modest but significant increase in risk of AD and early AD pathology in women homozygous for the ACE I-allele independent of vascular factors.

Original publication

DOI

10.1016/j.neurobiolaging.2004.09.011

Type

Journal article

Journal

Neurobiology of aging

Publication Date

08/2005

Volume

26

Pages

1153 - 1159

Addresses

Department of Epidemiology and Biostatistics, Erasmus Medical Center, Rotterdam, The Netherlands.

Keywords

Amygdala, Hippocampus, Nerve Fibers, Myelinated, Humans, Cerebrovascular Disorders, Alzheimer Disease, Atrophy, Genetic Predisposition to Disease, Peptidyl-Dipeptidase A, Magnetic Resonance Imaging, Cohort Studies, DNA Mutational Analysis, Sex Factors, Genotype, Homozygote, Polymorphism, Genetic, Aged, Middle Aged, Netherlands, Female, Male, Genetic Testing