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a Department of
Medical Genetics, Wellcome Trust Centre for Molecular Mechanisms in
Disease, Cambridge Institute for Medical Research, Wellcome/MRC
Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2XY,
UK, b Department of Public
Health and Primary Care, University Forvie Site, Robinson Way,
Cambridge CB2 2SR, UK, c CRC Genetic Epidemiology Unit, Cambridge
University Department of Public Health and Primary Care, Strangeways
Research Laboratory, Wort's Causeway, Cambridge CB1 8RN, UK, d Department
of Clinical Geratology, Radcliffe Infirmary, Oxford OX2 6HE, UK, e Department of Pathology,
Cambridge University, Addenbrooke's Hospital, Hills Road, Cambridge
CB2 2QQ, UK, f Medical
Research Council Brain Bank, Department of Neuropathology, Institute of
Psychiatry, De Crespigny Park, London SE5 8AF, UK, g Neuropathology Department, Radcliffe Infirmary,
Oxford OX2 6HE, UK
Correspondence to: Dr Rubinsztein, dcr1000{at}cus.cam.ac.uk
Revised version received 19 April 2000;
Accepted for publication 3 May
2000
A recent study suggested that the insertion (I) allele in
intron 16 of the angiotensin converting enzyme gene
(ACE) is associated with Alzheimer's
disease (AD) risk. In our series of 239 necropsy confirmed late onset
AD cases and 342 elderly non-demented controls aged >73 years, we
found significantly different ACE genotype distributions in the case and control groups (p=0.007). Homozygotes for
both the I and D alleles were associated with a higher risk compared to
DI heterozygotes. While the APOE
4 allele was strongly associated with AD risk in our series, we
found no evidence for an interaction between the
APOE and
ACE loci. In addition, no interactions were
observed between ACE and gender or age at
death of the AD cases. A meta-analysis of all published reports (12 case-control series in total) suggested that both the II and ID ACE genotypes are associated with increased
AD risk (odds ratio (OR) for II v DD 1.36, 95% confidence interval (CI)=1.13-1.63, OR for DI
v DD 1.33, 95% CI=1.14-1.53,
p=0.0002).
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