▎ 摘　　要

Alzheimer's disease (AD) is a common neurodegenerative disease, and its pathogenesis is closely related to beta-amyloid (A beta) peptide. The deposition of A beta in the brain due to impaired A beta clearance is considered as an important cause of AD. The decrease in A beta clearance is closely related to the autophagy dysfunction in brains of AD patients. It is feasible to treat AD by increasing the autophagy level of cells such as microglia and neurons to accelerate A beta clearance. In this article we explored the ability of graphene oxide (GO) to clear A beta through activating autophagy. Our work demonstrated that GO could inhibit the mTOR signaling pathway by activating AMPK to induce the autophagy of microglial and neurons. As expected, with the improvement of autophagy ability of microglia, GO promoted microglia-mediated A beta phagocytosis. Under the conditions of co-culture of microglia and neurons, GO induced the autophagy of microglia and neurons, especially the autophagy of microglia, thereby promoting the clearance of A beta, and ultimately achieved the effect of protecting neurons. Moreover, GO was not only non-cytotoxic to microglia and neurons but also able to reduce the toxicity of A beta to neurons through its clearance. These results have shown the potential of GO in treating Alzheimer's disease.