Given that: (1) autophagy is necessary for the degradation of Aβ in microglia, (2) p-AKT [20] and p-ERK [21] associate with Aβ-accumulation and tau phosphorylation in AD animal models [22,23], and (3) autophagy is modulated by D4T [19], we aimed to explore in more detail the mechanisms responsible for the D4T-mediated autophagy clearing of Aβ. Here, AKT1 is linked to Alzheimer disease.