Extracellular deposition of amyloid-β (Aβ) is one of the pathological hallmarks of Alzheimer's disease (AD) [1].It has emerged that innate immune activation plays an important role in AD and other neurodegenerative diseases[2].On the understanding of the interactions between Aβ and the innate immune system in the brain,it is well know that both fibrillary and oligomeric Aβ can activate the main innate immune cells,microglia,through multiple micro-glial receptors [2,3].Microglial activation may enhance the phagocytosis of Aβ for clearance.However,in response to Aβ,microglia produce pro-inflammatory cytokines,which induce Aβ deposition [3].Although it is known that the innate immune system is associated with Aβ deposi-tion,it is largely unknown how this system is linked to Aβ production,and which molecule mediates Aβ production.