认知障碍是糖尿病引起的严重并发症之一，导致痴呆及AD的风险显著增加。mTORC1既是胰岛素信号和营养物质代谢的枢纽，也是引起神经元CCR的上游启动因素。我们在前期研究中发现，肉桂多酚能改善糖尿病动物的认知能力，降低神经元mTORC1对下游靶点的活化水平，减少细胞周期蛋白的生成。因此我们认为，肉桂多酚治疗糖尿病认知障碍的机制可能是通过抑制mTORC1的活化，进而阻止神经元异常的CCR，减少神经元丢失。为阐明肉桂多酚的具体作用机制，本项目拟从分子相互作用层次开展分子垂钓，确认肉桂多酚与mTORC1的相互作用；在离体细胞层次通过定向调控mTORC1功能，证明肉桂多酚的作用对象及阻止CCR的效应；并在整体动物水平对肉桂多酚的作用机制进行检验。通过本项目的研究将为肉桂多酚治疗糖尿病认知障碍的作用提供更为有力的证据，为糖尿病认知障碍的治疗提供新的思路和备选药物。

Cognitive impairment is one of the serious complications of diabetes mellitus, leading to a significant rising risk of dementia and AD. MTORC1 is not only the hub of insulin signaling and nutrient metabolism, but also the upstream trigger of CCR in neurons. Our previous studies have revealed that cinnamon polyphenols improved the cognitive ability of diabetic animals, reduced the activation level of mTORC1 downstream targets in neuron, and reduced the production of cell cycle proteins. Therefore, we believe that the therapeutic mechanism of cinnamon polyphenols in the diabetic cognitive impairment lies in inhibiting the activation of mTORC1, thereby preventing abnormal CCR of neurons and reducing neuron loss. In order to elucidate the specific mechanism of cinnamon polyphenols, this project intends to carry out molecular fishing to illuminate the interaction between cinnamon polyphenols and mTORC1; and directional regulating mTORC1 function to prove the target of cinnamon polyphenols and its’ effect on preventing CCR in vitro; and verify the mechanism of cinnamon polyphenols in animal model of diabetic cognitive impairment. This study will provide more powerful evidence for the therapeutic effect of cinnamon polyphenols in diabetic cognitive impairment, and provide new ideas and alternative drugs for the treatment of diabetic cognitive impairment.