Accumulation of amyloid-β peptides (Aβ) in the brain triggers the onset of Alzheimer's disease (AD). Therefore, promotion of Aβ clearance is a promising strategy for AD therapy. We previously demonstrated that primary-cultured rat microglia phagocytose Aβ, and the transplantation with rat microglia ameliorates the Aβ burden in brains of Aβ-injected rats. In this study, we demonstrated that stimulation with colony-stimulating factor-1 (CSF-1) efficiently differentiated mouse bone marrow (BM) cells into BM-derived microglia-like (BMDML) cells. BMDML cells effectively phagocytosed Aβ in vitro, and it was comparable to that of primary-cultured mouse microglia. We further found that intra-hippocampally injected BMDML cells migrated directionally toward Aβ plaques in a mouse model of AD in comparisons with a simulation assuming a uniform distribution of cells. Finally, we detected Aβ phagocytosis by BMDML cells concomitant with a reduction in the number and area of Aβ plaques and amelioration of the cognitive impairment in the mouse model. Our results suggest that BMDML cells could be used in cell-based disease-modifying therapies against AD.