Liu et al. [130] also showed that in a double-transgenic mouse model of AD, the expression levels of miR-26b were increased, additionally finding that while the suppression of miR-26b in N2a/APP cells increased IGF- 1 protein levels and inhibited the synthesis of Aβ, the overexpression of miR-26b in N2a/APP cells downregulated IGF-1 protein expression levels and encouraged the creation of Aβ. This evidence concerns the gene APP and Alzheimer disease.