We further show that by crossing the hCSF1Bdes mouse to the AppSAA mouse model of AD and AppHu control mice, the xenografted hMG exposed to amyloid-β pathology in AppSAA upregulate the typical activation markers previously described, including CD9 and HLA-DQ/DR both on mRNA and protein levels, predominantly in the vicinity to plaques. This evidence concerns the gene CD9 and Alzheimer disease.