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. The gene discussed is APP; the disease is amyloidosis.