At first glance, these results are in contradiction to what we and others reported previously, when we observed that late-stage inhibition of CSF1R had no impact on plaque pathology, despite driving a beneficial impact on synaptic preservation and overall pathology in models of amyloidosis (Olmos-Alonso et al., 2016; Spangenberg et al., 2016; Dagher et al., 2015) or tau pathology (Mancuso et al., 2019). Here, CSF1R is linked to amyloidosis.