To investigate the role of microglia miR-155 in the APP/PS1 mouse model of AD, we crossed APPSwe/PS1dE9± (APP/PS1±) mice to generate APP/PS1± miR-155flx/flx CX3CR1CreER/+ mice and littermate controls (miR-155flx/flx CX3CR1CreER/+) that do not express mutated human-APP (Fig. 1A). This evidence concerns the gene APP and Alzheimer disease.