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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-61130

Bartl, J; Scholz, C J; Hinterberger, M; Jungwirth, S; Wichart, I; Rainer, M K; Kneitz, S; Danielczyk, W; Tragl, K H; Fischer, P; Riederer, P; Grünblatt, E (2011). Disorder-specific effects of polymorphisms at opposing ends of the Insulin Degrading Enzyme gene. BMC Medical Genetics, 12(12):151.

Published Version



Insulin-degrading enzyme (IDE) is the ubiquitously expressed enzyme responsible for insulin and amyloid beta (Aβ) degradation. IDE gene is located on chromosome region 10q23-q25 and exhibits a well-replicated peak of linkage with Type 2 diabetes mellitus (T2DM). Several genetic association studies examined IDE gene as a susceptibility gene for Alzheimer's disease (AD), however with controversial results.

We examined associations of three IDE polymorphisms (IDE2, rs4646953; IDE7, rs2251101 and IDE9, rs1887922) with AD, Aβ42 plasma level and T2DM risk in the longitudinal Vienna Transdanube Aging (VITA) study cohort.

The upstream polymorphism IDE2 was found to influence AD risk and to trigger the Aβ42 plasma level, whereas the downstream polymorphism IDE7 modified the T2DM risk; no associations were found for the intronic variant IDE9.

Based on our SNP and haplotype results, we delineate the model that IDE promoter and 3' untranslated region/downstream variation may have different effects on IDE expression, presumably a relevant endophenotype with disorder-specific effects on AD and T2DM susceptibility.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Child and Adolescent Psychiatry
DDC:610 Medicine & health
Deposited On:10 Mar 2012 17:17
Last Modified:05 Dec 2013 16:15
Publisher:BioMed Central
Publisher DOI:10.1186/1471-2350-12-151
PubMed ID:22107728
Citations:Web of Science®. Times Cited: 2
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Scopus®. Citation Count: 1

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