自噬可以介导小胶质细胞对细胞外Aβ的清除作用，诱导小胶质细胞自噬对阿尔茨海默病防治具有重要意义，但是在阿尔茨海默病(AD)发病条件下诱导小胶质细胞自噬的作用靶点不明确。.我们在制备卡拉胶寡糖（KOS）的基础上，发现KOS具有诱导小胶质细胞自噬和降低神经炎症的双重功能，因此本项目拟以KOS作为探针化合物，以小胶质细胞和AD小鼠作为研究对象，以AMPK/ULK1自噬调控途径为切入点，通过蛋白印迹、siRNA干扰、细胞混合培养等技术，研究KOS诱导小胶质细胞自噬的的作用途径和位点，探讨KOS诱导自噬与抑制炎症之间的相互作用规律，揭示KOS通过诱导小胶质细胞自噬对神经损伤的保护机制。项目最终不仅将阐明KOS基于AMPK/ULK1通路诱导小胶质细胞自噬的作用机理，而且能够明确AMPK/ULK1通路中调控小胶质细胞自噬的关键因子和作用靶点，为以诱导小胶质细胞自噬为靶标的AD治疗和药物筛选提供科学依据。

Some resent research works showed that autophagy of microglia can mediate the degradation of extracellular Aβ and induction of autophagy has been regarded as a new therapeutic target for Alzheimer's disease (AD), but the target point of inducting the autophagy of microglia under the progress of AD is still unrevealed..Our previous work showed that carrageenan oligosaccharides (KOS), which were prepared in our lab, can induce autophagy of microglia and inhibit neuroinflammation. But there still are some unsolved issues which are barriers for us to understand the mechanism of autophagy induced by KOS, such as the regulation pathway of autophagy induced by KOS, the interaction between the autophagy induction and inhibition of neuroinflammation and the neuroprotection through the autophagy induced by KOS. In order to solve above issues, our project will use KOS as probe compound and focus on the AMPK/ULK1 pathway of the microglia autophagy to explore the regulation signal pathway of autophagy and the neuroprotection induced by KOS with methods of western blotting, siRNA and co-culture cell et al. At the end, the mechanism of autophagy induced by KOS, the interaction between autophagy induction and neuroinflammation inhibition and the neuroprotection by increasing autophagy will be revealed in our project. The key factor and target point for the regulation of microglia autophagy through the AMPK/ULK1 pathway will be identified in this project. All results of this project will provide scientific basis for the AD treatment and drug screening with the target of the induction of microglia autophagy.