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Background  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.    Methods  We examined associations of three  IDE  polymorphisms (IDE2, rs4646953; IDE7, rs2251101 and IDE9, rs1887922) with AD, Aβ 42  plasma level and T2DM risk in the longitudinal Vienna Transdanube Aging (VITA) study cohort.    Results  The upstream polymorphism IDE2 was found to influence AD risk and to trigger the Aβ 42  plasma level, whereas the downstream polymorphism IDE7 modified the T2DM risk; no associations were found for the intronic variant IDE9.    Conclusions  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.

Disorder-specific effects of polymorphisms at opposing ends of the Insulin Degrading Enzymegene