{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T08:07:11Z","timestamp":1792397231553,"version":"4.4.0"},"reference-count":15,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2002,1,9]],"date-time":"2002-01-09T00:00:00Z","timestamp":1010534400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am. J. Med. Genet."],"published-print":{"date-parts":[[2002,4,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>ApoE<\/jats:italic> \u03f54 allele increases the risk of late\u2010onset Alzheimer disease (AD) as well as the amount of beta\u2010amyloid deposition in the brain. Because half of AD patients do not have <jats:italic>ApoE<\/jats:italic> \u03f54, it is important to search for other determinants of <jats:italic>ApoE<\/jats:italic> that modify AD risk. We tested whether the haplotype background of the most common <jats:italic>ApoE<\/jats:italic> allele, \u03f53, influences brain amyloid deposition or the risk of neuropathologically verified AD in a population\u2010based sample of elderly Finns. To exclude the effects of ApoE protein polymorphism we focused these analyses on subjects homozygous for \u03f53. Haplotypes were defined using polymorphisms at positions \u2212\u2009491 and \u2212\u2009219 of the <jats:italic>ApoE<\/jats:italic> promoter and at position +113 of intron\u20101. We found that \u03f53\u2010haplotypes containing the promoter allele \u2212\u2009219T were associated with reduced amyloid deposition and reduced risk of neuropathologically verified AD as compared to \u03f53\u2010haplotypes containing \u2212\u2009219G. The functional polymorphism(s) responsible for the haplotypic difference remains to be identified. These results indicate that there is significant allelic variation in the <jats:italic>ApoE<\/jats:italic> gene region, which modulates brain amyloid deposition and AD risk, independent of the ApoE protein polymorphism. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajmg.10202","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T23:13:41Z","timestamp":1030317221000},"page":"288-291","source":"Crossref","is-referenced-by-count":23,"title":["<i>ApoE<\/i> \u03f53\u2010haplotype modulates Alzheimer beta\u2010amyloid deposition in the 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