They used AppNl-G-f mice which carry three APP knockout mutations with familial AD causing elevated levels of Aβ42 and observed decreased amyloid deposition, a decline in P-tau-positive areal fraction in the hippocampus (p< 0.001), increased activation of microglial in the area of amyloid deposition (p < 0.001) and a significantly higher mean Parvalbumin-positive (PV+) neuron density (p = 0.019) in the AST group over the control group. Here, APP is linked to Alzheimer disease.