Animals were injected at the age of 3 months and evaluated 3 months later (i.e. at 6 months of age), a time point at which APP/PS1 mice normally exhibit ongoing amyloid pathology but no memory deficits.39,40 Strikingly, we observed, using Y-maze and Barnes maze, that at such an early time point, spatial memory was strongly impaired in APP/PS1 mice overexpressing neuronal A2AR—as it is expected to occur at later time points in APP/PS1 mice—when compared with the other littermate groups (WT, A2A and APP/PS1), which exhibited proper memory abilities. This evidence concerns the gene APP and amyloidosis.