APP and Alzheimer disease: Moreover, to assess the changes of miR-200a-3p expression during AD progression, SH-SY5Y cells overexpressing the APPswe plasmid and two mouse models, the APP/PS1 transgenic and the mutant SAMP8 strains, were used because they have been previously shown to express deficits closely similar to AD (Ding et al., 2008; Liu et al., 2012; Takagane et al., 2015).