Altogether, these findings highlight the strong associationbetween initial Aβ pathology and EAAT2 dysfunction in AD, eitherin a direct manner (AβOs-induced decrease on EAAT2 levels byphysical interaction and internalization of EAAT2 in the membraneof astrocytes or via downstream signaling pathways, e.g., CN/NFATpathway103) or by alternative mechanismsassociated with Aβ aggregation, such as cholesterol dyshomeostasis(a catalyzer of Aβ aggregation process104) and PS1 expression (associated with APP cleavage and Aβ formation). This evidence concerns the gene APP and Alzheimer disease.