Importantly, the specificity of Tn‐R's regulatory role was highlighted by the absence of significant alterations in GFAP‐positive astrocyte populations after Tn‐R downregulation (Figure S7 in supporting information), indicating that Tn‐R primarily mediates microglial response to Aβ pathology rather than influencing astrocytic activation in the APP/PS1 AD model. This evidence concerns the gene GFAP and Alzheimer disease.