{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T20:24:07Z","timestamp":1775593447085,"version":"3.50.1"},"reference-count":8,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2001,1,1]],"date-time":"2001-01-01T00:00:00Z","timestamp":978307200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2001,1,1]],"date-time":"2001-01-01T00:00:00Z","timestamp":978307200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Dement Geriatr Cogn Disord"],"published-print":{"date-parts":[[2001]]},"abstract":"Apolipoprotein E <i>(APOE)<\/i> has been extensively demonstrated to be a genetic risk factor for Alzheimer\u2019s disease (AD). Associations of <i>APOE<\/i> genotype have been reported with age at AD onset, rate of decline, and responsiveness to therapy. This study aimed to test these hypotheses in a large study population of AD patients. <i>APOE<\/i> genotype was determined from 1,528 Caucasian subjects, diagnosed by NINCDS\/ADRDA criteria as probable AD patients, enrolled in four international placebo-controlled clinical trials of 3\u201312 months duration, designed to evaluate efficacy of treatment with galantamine or sabeluzole. In addition to patient demographics and baseline scores for Mini Mental State Examination, scores on the Disability Assessment for Dementia (DAD) and the cognitive subscale of the Alzheimer\u2019s Disease Assessment Scale (ADAS-cog) were recorded at the start, during, and at the end of the study. <i>APOE<\/i> &#917;4 homozygotes had a significantly lower age at disease onset compared to patients with other <i>APOE<\/i> genotypes. The &#917;4 allele was significantly over-represented in females compared to males, and in the group of subjects with an AD family history. Based on longitudinal data of 504 placebo-treated AD patients, the linear annual rate of change in score was 5 points on the ADAS-cog scale and 11 on the DAD scale. The &#917;4 allele copy number did not influence these rates of decline. Sabeluzole treatment was not effective in the overall group compared to the placebo-treated group, nor in any subgroup stratified by &#917;4 allele count. Galantamine produced cognitive and functional improvement that were not affected by &#917;4 allele count. In conclusion, our data confirm a strong association between &#917;4 homozygotes and age at onset of AD but do not support an effect of &#917;4 allele copy number on rate of cognitive and functional decline nor on the efficacy of galantamine in patients with AD.<\/jats:p>","DOI":"10.1159\/000051238","type":"journal-article","created":{"date-parts":[[2003,4,15]],"date-time":"2003-04-15T12:11:24Z","timestamp":1050408684000},"page":"69-77","source":"Crossref","is-referenced-by-count":66,"title":["<i>APOE<\/i> Genotype: No Influence on Galantamine Treatment Efficacy Nor on Rate of Decline in Alzheimer\u2019s Disease"],"prefix":"10.1159","volume":"12","author":[{"given":"Jeroen","family":"Aerssens","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Raeymaekers","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sean","family":"Lilienfeld","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hugo","family":"Geerts","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frank","family":"Konings","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wim","family":"Parys","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2001,2,9]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199802193380804"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(93)91705-Q"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(97)80089-X"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016\/0022-3956(75)90026-6"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.55.7.964"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1038\/ng0694-180"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1159\/000017034"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)93288-X"}],"container-title":["Dementia and Geriatric Cognitive Disorders"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/51238","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/51238","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:03:16Z","timestamp":1745467396000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000051238"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2001]]},"references-count":8,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2001,4,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000051238","archive":["Portico"],"relation":{},"ISSN":["1420-8008","1421-9824"],"issn-type":[{"value":"1420-8008","type":"print"},{"value":"1421-9824","type":"electronic"}],"subject":[],"published":{"date-parts":[[2001]]}}}