Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4328806 | Brain Research | 2009 | 8 Pages |
Abstract
Cerebral accumulation of amyloid beta protein (Aβ) is believed to play a central role in the pathogenesis of Alzheimer's disease (AD). Insulin degrading enzyme (IDE) is involved in Aβ degradation, therefore the gene encoding for insulin degrading enzyme is one of the candidate genes risky for AD. In Chinese Han populations we found three polymorphisms in IDE promoter: â1002T/G (rs3758505), â179T/C (rs4646953) and â51C/T (rs4646954). The â1002T and â51C alleles were over-represented in 357 sporadic AD (SAD) patients when compared to those in 331 healthy individuals. Furthermore, â1002T/G and â51C/T were in strong linkage disequilibrium and they constructed a relatively risky â1002T/â51C and a relatively protective â1002G/â51T. Luciferase reporter assay indicated â1002T/â51C had lower transcriptional activity than â1002G/â51T. A more marked increase in â1002T/â51C transcriptional activity was seen when under Aβ25-35 and serum deprivation treatment. The present study provides evidence that IDE promoter polymorphisms that significantly decrease IDE expression levels are associated with development of SAD.
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Authors
Xiumei Zuo, Jianping Jia,