We sought to answer the question: Would ten days of CSF1R inhibition in the early stage of amyloidosis significantly deplete activated microglia in 5xFAD mouse brain, resulting in residual microglia exhibiting a noninflammatory phenotype characterized by highly ramified processes, reduced NLRP3 inflammasome complexes and mTOR signaling, and improved metabolic fitness? This evidence concerns the gene CSF1R and amyloidosis.