This discrepancy between these two animal models of AD can be explained by the fact that the FAβ1–42 infusion model represents a model of inflammation induced by the direct exposition of hippocampal tissues to FAβ1–42 peptide loads [71], while the APPswe/PS1dE9 transgenic model corresponds to a model of chronic inflammation induced by the gradual accumulation of Aβ deposits over the lifespan of transgenic animals, which express constitutive mutant forms of APP and PS1 [72]. Here, PSEN1 is linked to Alzheimer disease.