{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T18:50:15Z","timestamp":1792349415934,"version":"4.4.0"},"reference-count":43,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":3051,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1996,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Alzheimer's Disease (AD) is a complex genetic disorder with four loci already identified. Mutations in three of these, the amyloid precursor protein, presenilin I, and preseuilin II, cause early\u2010onset AD. The apolipoprotein E (APOE) gene contributes primarily to late\u2010onset AD. The APOE\u20104 allele acts in a doserelated fashion to increase risk and decrease the age\u2010of\u2010onset distribution in AD. We examined the effect of APOE on AD in a previously unstudied Amish population that has a lower prevalence of dementia compared with other populations. We sampled a large inbred family with 6 latehyphen: onset AD members. We also genotyped 53 individuals from the general Amish population as controls for the APOE allele frequency estimates. The frequency of the APOE\u20104 allele in the Amish controls was 0.037 \u00b1 0.02. This differed significantly compared with three independent sets of non\u2010Amish white controls (<jats:italic>p<\/jats:italic> &lt; 2 \u00d7 10\u22124, <jats:italic>p<\/jats:italic> &lt; 6 \u00d7 10\u22125, and <jats:italic>p<\/jats:italic> &lt; 2 \u00d7 10\u22126). In addition, all Amish AD\u2010affected individuals had APOE 3\/3 genotypes; no APOE X\/4 or 4\/4 individuals were observed. We suggest that the lower frequency of dementia in the Amish may be partially explained by the decreased frequency of the APOE\u22124 allele in this population, and that the inbred nature of this pedigree, with its strong clustering of cases contrasted against the lower frequency of dementia, indicates that additional genetic factors influence late\u2010onset AD.<\/jats:p>","DOI":"10.1002\/ana.410390605","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T14:46:04Z","timestamp":1104590764000},"page":"700-704","source":"Crossref","is-referenced-by-count":46,"title":["Alzheimer's disease and apolipoprotein e\u20104 allele in an amish population"],"prefix":"10.1002","volume":"39","author":[{"given":"M. A.","family":"Pericak\u2010Vance","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. C.","family":"Johnson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. B.","family":"Rimmler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. M.","family":"Saunders","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. C.","family":"Robinson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. G.","family":"D'Hondr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. E.","family":"Jackson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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