Alzheimer's disease (AD) is the most common cause of dementia. AD treatments currently approved are commonly regarded as purely symptomatic. Therefore, development of effective disease modifying treatments is eagerly required. Pathological hallmarks of AD brain include amyloid-β (Aβ) accumulation, neurofibrillary tangle (NFT), synaptic loss, and neurodegeneration. Understanding of AD pathogenesis provides deep insight into the therapeutic approach for AD. In this review, we introduce our current translational researches for new therapeutic strategies against AD. We recently revealed that a key molecule for actin assembly, Wiscott-Aldrich syndrome protein family verprolin-homologous protein (WAVE), is accumulated into NFT in an Aβ pathology-dependent manner. Because synaptic function is maintained by precise regulation of actin assembly, abnormal accumulation of WAVE induced by Aβ pathology may expand the NFT pathology to synaptic dysfunction. These results imply that lowering of brain Aβ at the early stage of AD pathogenesis is a promising therapeutic approach. As the approach for the elimination of brain Aβ, we have studied microglial Aβ phagocytosis and proposed its therapeutic application for AD treatment. We demonstrated that anti-Aβ antibody and galantamine promote microglial Aβ phagocytosis by binding to Fc receptors and nicotinic acetylcholine receptors on microglia, respectively. On the other hand, we demonstrated that the transplantation with microglia effectively eliminate brain Aβ and microglia-like Aβ phagocytic cells were successfully prepared from bone marrow derived cells by the stimulation with macrophage colony-stimulating factor. Thus, we have studied cell therapeutic strategy aim at its clinical application for AD treatment by the activation of endogenous microglia and transplantation of exogenous microglia-like Aβ phagocytic cells.