SLC1A2 and Alzheimer disease: 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).