{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,28]],"date-time":"2023-10-28T14:49:07Z","timestamp":1698504547758},"reference-count":20,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":2594,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1997,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We examined the association of apolipoprotien E (ApoE) genotype and the risk of early\u2010onset Alzheimer's disease (AD) in 209 white early\u2010onset sporadic cases (43% male) and 303 white controls (48% male) of similar age distribution. The risk of AD was significantly increased, relative to the 3\/3 genotype, in people with the 4\/4, 3\/4, and 2\/4 genotypes, controlling for age at time of examination and sex. The 2\/3 genotype reduced slightly the risk of AD, although the effect was not statistically significant. We conclude, contrary to some previous reprots, that the ApoE \u03b52 allele does not increase the risk of early\u2010onset sporadic AD.<\/jats:p>","DOI":"10.1002\/ana.410420317","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T15:04:16Z","timestamp":1104591856000},"page":"376-378","source":"Crossref","is-referenced-by-count":6,"title":["Apolipoprotein E \u03b52 does not increase risk of early\u2010onset sporadic Alzheimer's disease"],"prefix":"10.1002","volume":"42","author":[{"given":"W. K.","family":"Scott","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. 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