{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:11:38Z","timestamp":1762099898786,"version":"build-2065373602"},"reference-count":6,"publisher":"BMJ","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Med Genet"],"published-print":{"date-parts":[[2001,4,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVES<\/jats:title>\n                  <jats:p>The only locus unequivocally associated with late onset Alzheimer's disease (AD) risk is <jats:italic>APOE<\/jats:italic>. However, this locus accounts for less than half the genetic variance. A recent study suggested that the A allele of the 3\u2032UTR biallelic polymorphism in the<jats:italic>LBP-1c<\/jats:italic>\/<jats:italic>CP2<\/jats:italic>\/<jats:italic>LSF<\/jats:italic>gene 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.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec sec-type=\"methods\">\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>The 3\u2032UTR polymorphism in the<jats:italic>LBP-1c<\/jats:italic>\/<jats:italic>CP2<\/jats:italic>\/<jats:italic>LSF<\/jats:italic>gene was typed in 216 necropsy confirmed AD cases and 301 non-demented controls aged &gt;73 years.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>We found different<jats:italic>LBP-1c<\/jats:italic>\/<jats:italic>CP2<\/jats:italic>\/<jats:italic>LSF<\/jats:italic>allele 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 \u03b54 carrier status.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Our data support<jats:italic>LBP-1c<\/jats:italic>\/<jats:italic>CP2<\/jats:italic>\/<jats:italic>LSF<\/jats:italic>as a candidate gene\/risk factor for AD and provide justification for future studies to investigate the role of this gene in Alzheimer's disease.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/jmg.38.4.232","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T06:38:40Z","timestamp":1027751920000},"page":"232-233","source":"Crossref","is-referenced-by-count":22,"title":["Genetic association of an<i>LBP-1c<\/i>\/<i>CP2<\/i>\/<i>LSF<\/i>gene polymorphism with late onset Alzheimer's disease: Table 1"],"prefix":"10.1136","volume":"38","author":[{"given":"Alison E","family":"Taylor","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Agustin","family":"Yip","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carol","family":"Brayne","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Douglas","family":"Easton","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John Grimley","family":"Evans","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Xuereb","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nigel","family":"Cairns","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Margaret M","family":"Esiri","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David C","family":"Rubinsztein","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2001,4,1]]},"reference":[{"key":"2025101711474699000_38.4.232.1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1997.03550160069041"},{"key":"2025101711474699000_38.4.232.2","doi-asserted-by":"publisher","DOI":"10.1159\/000017120"},{"key":"2025101711474699000_38.4.232.3","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.hmg.a018918"},{"key":"2025101711474699000_38.4.232.4","first-page":"319","article-title":"Cognitive function and dementia in six areas of England and Wales: the distribution of MMSE and prevalence of GMS organicity level in the MRC CFA study.","volume":"28","year":"1999","journal-title":"Psychol Med"},{"key":"2025101711474699000_38.4.232.5","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.1994.03950040069009"},{"key":"2025101711474699000_38.4.232.6","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.37.9.695"}],"container-title":["Journal of Medical Genetics"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/syndication.highwire.org\/content\/doi\/10.1136\/jmg.38.4.232","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,10,17]],"date-time":"2025-10-17T18:47:55Z","timestamp":1760726875000},"score":1,"resource":{"primary":{"URL":"https:\/\/jmg.bmj.com\/lookup\/doi\/10.1136\/jmg.38.4.232"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2001,4,1]]},"references-count":6,"journal-issue":{"issue":"4","published-online":{"date-parts":[[2001,4,1]]},"published-print":{"date-parts":[[2001,4,1]]}},"alternative-id":["10.1136\/jmg.38.4.232"],"URL":"https:\/\/doi.org\/10.1136\/jmg.38.4.232","relation":{},"ISSN":["0022-2593","1468-6244"],"issn-type":[{"type":"print","value":"0022-2593"},{"type":"electronic","value":"1468-6244"}],"subject":[],"published":{"date-parts":[[2001,4,1]]}}}