The analyzed polymorphisms should serve as proxies to partly capture the common allelic variation in the up- (IDE2) and downstream (IDE7) region, as well as in the gene body (IDE9) of IDE. Our finding that we were not able to detect associations of IDE9 with neither examined trait leads us to the hypothesis that common IDE variants influencing the primary structure of the IDE protein (i.e. non-synonymous SNPs and those affecting splicing junctions, respectively) may have no major impact on AD and T2DM susceptibility. Here, IDE is linked to Alzheimer disease.