{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T03:00:37Z","timestamp":1791255637457,"version":"4.1.0"},"reference-count":17,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":3994,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1993,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Apolipoproein E (APO\u2010E) binds to the \u03b2\u2010amyloid peptide and is present in senile neuritic plaques in Alzheimer's disease (AD). The \u03b54 isoform of APO\u2010E has been associated with both sporadic and familial late\u2010onset AD, implying a causal role. Among patients and control subjects similar in age, gender, and ethnic group from the New York City community of Washington Heights\u2010Inwood, we found that the odds ratio (OR) for AD associated with homozygosity for APO\u2010\u03b54 was 17.9 (95% confidence interval [CI], 4.6\u201369.8) and that associated with heterozygosity for APO\u2010\u03b54 was 4.2 (95% CI, 1.8\u20139.5), compared with persons with other APO\u2010E genotypes. The association was stronger among patients with sporadic disease (OR = 10.3; 95% CI, 3.4\u201331.1) than among those with a family history of dementia in a first\u2010degree relative (OR = 0.9; 95% CI, 0.1\u201313.5). The association between APO\u2010\u03b54 and AD did not differ according to age at onset (&lt;65 vs \u226565), but appeared to vary across the 3 ethnic groups investigated (black, Hispanic, and white). Our data confirm the association between AD and APO\u2010\u03b54 and support the hypothesis that the APO\u2010\u03b54 allele either confers genetic susceptibility to AD or may be in linkage disequilibrium with another susceptibility locus. Ethnic variability in the allelic frequency of APO\u2010\u03b54 in the elderly warrants further investigation.<\/jats:p>","DOI":"10.1002\/ana.410340527","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T00:27:57Z","timestamp":1104539277000},"page":"752-754","source":"Crossref","is-referenced-by-count":319,"title":["The apolipoprotein \u03b54 allele in patients with Alzheimer's disease"],"prefix":"10.1002","volume":"34","author":[{"given":"Richard","family":"Mayeux","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaakov","family":"Stern","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth","family":"Ottman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas K.","family":"Tatemichi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming\u2010Xin","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gladys","family":"Maestre","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Colleen","family":"Ngai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin","family":"Tycko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henry","family":"Ginsberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2004,10,8]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.43.8.1467"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.5.1977"},{"key":"e_1_2_1_4_2","first-page":"1034","article-title":"Linkage studies in familial Alzheimer disease: evidence for chromosome 19 linkage","volume":"48","author":"Pericak\u2010Vance MA","year":"1991","journal-title":"Am J Hum Genet"},{"key":"e_1_2_1_5_2","first-page":"205","volume-title":"Diagnostic and statistical manual of mental disorders, third edition\u2010revised","author":"American Psychiatric Association","year":"1987"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.34.7.939"},{"key":"e_1_2_1_7_2","doi-asserted-by":"crossref","first-page":"545","DOI":"10.1016\/S0022-2275(20)43176-1","article-title":"Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhAI","volume":"31","author":"Hixson J","year":"1991","journal-title":"J Lipid Res"},{"key":"e_1_2_1_8_2","first-page":"160","volume-title":"Statistical methods for rates and proportions, ed 2","author":"Fleiss JL","year":"1981"},{"key":"e_1_2_1_9_2","volume-title":"Applied logistic regression","author":"Hosmer DW","year":"1989"},{"key":"e_1_2_1_10_2","first-page":"49","article-title":"Genetic studies of human apolipoproteins. 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