PT - JOURNAL ARTICLE AU - Alison E Taylor AU - Agustin Yip AU - Carol Brayne AU - Douglas Easton AU - John Grimley Evans AU - John Xuereb AU - Nigel Cairns AU - Margaret M Esiri AU - David C Rubinsztein TI - Genetic association of an<em>LBP-1c</em>/<em>CP2</em>/<em>LSF</em>gene polymorphism with late onset Alzheimer's disease AID - 10.1136/jmg.38.4.232 DP - 2001 Apr 01 TA - Journal of Medical Genetics PG - 232--233 VI - 38 IP - 4 4099 - http://jmg.bmj.com/content/38/4/232.short 4100 - http://jmg.bmj.com/content/38/4/232.full SO - J Med Genet2001 Apr 01; 38 AB - 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 &gt;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.