AIF1 and amyloidosis: These data suggest that the depleted microglia might not have been a major contributor to amyloid plaque degradation at this stage of disease pathology or that the remaining PLX5622 resistant Iba1+ cells in APP-PS1 mice are highly efficient in amyloid phagocytosis and able to compensate the low numbers of microglia thereby keeping the plaque load at the same level.