Reductions in NLRP3 inflammasome complexes in the residual microglia following 10 days of CSF1R inhibition in the early stage of AD are beneficial because NLRP3 inflammasome activation perpetuates chronic neuroinflammation and progression of AD pathogenesis (Bai & Zhang, 2021; Ising et al., 2019). This evidence concerns the gene CSF1R and Alzheimer disease.