Premium
No association between the insulin degrading enzyme gene and Alzheimer's disease in a Japanese population
Author(s) -
Sakai Ayumu,
Ujike Hiroshi,
Nakata Kenji,
Takehisa Yasushi,
Imamura Takaki,
Uchida Naohiko,
Kanzaki Akihiro,
Yamamoto Mitsutoshi,
Fujisawa Yoshikatsu,
Okumura Kazuya,
Kuroda Shigetoshi
Publication year - 2003
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.20106
Subject(s) - genetics , single nucleotide polymorphism , biology , gene , intron , apolipoprotein e , genetic association , chromosome , population , genotype , disease , medicine , environmental health
Susceptibility to Alzheimer's disease (AD) is thought to be regulated by multiple genetic factors. Recently, three independent studies have reported that loci on chromosome 10q are linked with AD, and the insulin degrading enzyme (IDE; MIM 146680) gene located on chromosome 10q23‐q25; IDE is located close to the maker D10S583, which exhibits a maximum LOD score for late‐onset AD. We examined seven polymorphisms in the IDE gene, the marker D10S583 in the 5′ flanking region, and SNPs in introns 1, 3, 11, 20, 21, and 22 (rs#1999764, 1855915, 1970244, 538469, 551266, and 489517, respectively). Four SNPs in introns 3, 11, 20, and 22 did not exhibit any polymorphisms in the Japanese population that was studied. D10S583 and two SNPs in introns 1 and 21 did not exhibit a significant association with early‐ or late‐onset AD. In addition, no associations were observed for subgroups of AD grouped according to APOE status. The present study indicates that the IDE gene polymorphisms do not confer susceptibility to early‐ or late‐onset AD at least in a Japanese population. © 2003 Wiley‐Liss, Inc.