@article {Taylor232, author = {Alison E Taylor and Agustin Yip and Carol Brayne and Douglas Easton and John Grimley Evans and John Xuereb and Nigel Cairns and Margaret M Esiri and David C Rubinsztein}, title = {Genetic association of anLBP-1c/CP2/LSFgene polymorphism with late onset Alzheimer{\textquoteright}s disease}, volume = {38}, number = {4}, pages = {232--233}, year = {2001}, doi = {10.1136/jmg.38.4.232}, publisher = {BMJ Publishing Group Ltd}, abstract = {OBJECTIVES The only locus unequivocally associated with late onset Alzheimer{\textquoteright}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{\textquoteright}s disease.}, issn = {0022-2593}, URL = {https://jmg.bmj.com/content/38/4/232}, eprint = {https://jmg.bmj.com/content/38/4/232.full.pdf}, journal = {Journal of Medical Genetics} }