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Age and Ageing Advance Access published online on November 24, 2009
Age and Ageing, doi:10.1093/ageing/afp210
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© The Author 2009. Published by Oxford University Press on behalf of the British Geriatrics Society.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

APOE and ACE polymorphisms and dementia risk in the older population over prolonged follow-up: 10 years of incidence in the MRC CFA Study

H.A.D. Keage1, F.E. Matthews2, A. Yip3, L. Gao2, C. McCracken4, I.G. McKeith5, D.C. Rubinsztein6, C. Brayne1 and MRC Cognitive Function and Ageing Study1

1 Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 0SR, UK
2 MRC Biostatistics Unit, Cambridge CB2 0SR, UK
3 Warren Alpert Medical School of Brown University, Providence, RI 02912 USA
4 School of Population, Community and Behavioural Sciences, University of Liverpool, Liverpool L69 3GA, UK
5 Institute for Ageing and Health, University of Newcastle, Newcastle upon Tyne NE2 4HH, UK
6 Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge CB2 2XY, UK

Address correspondence to: H.A.D. Keage; Email: hk323{at}medschl.cam.ac.uk.

Background: dementia risk conferred by apolipoprotein-E (APOE) and angiotensin-1-converting enzyme (ACE) polymorphisms have been reported for the MRC Cognitive Function and Ageing Study (CFAS) at 6-year follow-up. We concentrate on incident dementia risk over 10 years.

Methods: participants come from MRC CFAS, a multi-centre longitudinal population-based study of ageing in England and Wales. Three follow-up waves of data collection were used: 2, 6 and 10 years. Logistic regressions were undertaken to investigate associations between APOE (n = 955) and ACE (n = 856) alleles/genotypes and incident dementia. Two types of control groups were used: non-demented and highly functioning non-demented. Results were back-weighted.

Results: compared to APOE {varepsilon}3, {varepsilon}2 conferred protection of odds ratio (OR) = 0.3 (95% confidence interval, CI = 0.1–0.6) and {varepsilon}4 risk of OR = 2.9 (95% CI = 1.7–4.9) for incident dementia. Compared to {varepsilon}3/{varepsilon}3, the {varepsilon}3/{varepsilon}4 and {varepsilon}4/{varepsilon}4 genotypes conferred risks of OR = 3.6 (95% CI = 1.8–7.3) and OR = 7.9 (95% CI = 1.6–39.2), respectively. The {varepsilon}3/{varepsilon}2 genotype protected against dementia (OR = 0.2, 95% CI = 0.1–0.7), and {varepsilon}2/{varepsilon}2 had a similar protective effect but with wide CIs (OR = 0.3, 95% CI = 0.1–1.7). Restricting the control group accentuated these differentials. The effects of ACE alleles/genotypes on incident dementia risk were small.

Conclusions: APOE but not ACE is associated with late-onset incident dementia in the population. Using longer term follow-up with proper adjustment for attrition and incident cases increases estimates of risk.

Keywords: apolipoprotein-E, angiotensin-1-converting enzyme, population, dementia, old

Received 5 March 2009; accepted in revised form 19 October 2009.


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