Genetic association of anLBP-1c/CP2/LSFgene polymorphism with late onset Alzheimer's disease
- Alison E Taylora,b,
- Agustin Yipa,c,
- Carol Braynec,
- Douglas Eastond,
- John Grimley Evanse,
- John Xuerebf,
- Nigel Cairnsg,
- Margaret M Esirih,
- David C Rubinszteina
- aDepartment 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, bDepartment of Medical Genetics, Molecular Genetics Laboratory, Box 158 Addenbrooke's NHS Trust, Hills Road, Cambridge CB2 2QQ, UK, cDepartment of Public Health and Primary Care, University Forvie Site, Robinson Way, Cambridge CB2 2SR, UK, dCRC Genetic Epidemiology Unit, Cambridge University Department of Public Health and Primary Care, Strangeways Research Laboratory, Wort's Causeway, Cambridge CB1 8RN, UK, eDepartment of Clinical Geratology, Radcliffe Infirmary, Oxford OX2 6HE, UK, fDepartment of Pathology, Cambridge University, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK, gMedical Research Council Brain Bank, Department of Neuropathology, Institute of Psychiatry, London, De Crespigny Park, London SE5 8AF, UK , hNeuropatholology Department, Radcliffe Infirmary, Oxford OX2 6HE, UK
- Dr Rubinsztein,dcr1000{at}cus.cam.ac.uk
- Revised 17 January 2001
- Accepted 18 January 2001
Abstract
OBJECTIVES The only locus unequivocally associated with late onset Alzheimer's disease (AD) risk is APOE. However, this locus accounts for less than half the genetic variance. A recent study suggested that the A allele of the 3′UTR biallelic polymorphism in theLBP-1c/CP2/LSFgene was associated with reduced AD risk. Samples were diagnosed predominantly by clinical rather than pathological criteria. We have sought to replicate this finding in a series of necropsy confirmed, late onset AD cases and non-demented controls.
METHODS The 3′UTR polymorphism in theLBP-1c/CP2/LSFgene was typed in 216 necropsy confirmed AD cases and 301 non-demented controls aged >73 years.
RESULTS We found differentLBP-1c/CP2/LSFallele distributions in our AD cases and controls (p=0.048); the A allele was associated with reduced AD risk. The allele and genotype frequencies observed in our cases and controls were similar to those previously reported. No significant effects emerged when the data were adjusted for age, sex, or apoE ε4 carrier status.
CONCLUSIONS Our data supportLBP-1c/CP2/LSFas a candidate gene/risk factor for AD and provide justification for future studies to investigate the role of this gene in Alzheimer's disease.
