氧化损伤是导致AD发生的重要机制之一，通过饮食摄入抗氧化物质改善机体的抗氧化功能是预防AD的有效途径。课题组前期的研究证实，膳食来源的黄酮类物质可拮抗Aβ诱导的实验动物学习记忆损伤及神经细胞氧化损伤；GSTM1/GSTT1基因多态性、富含黄酮类物质膳食摄入与机体抗氧能力之间存在交互作用。由于GSTM1/GSTT1基因多态性可影响机体抗氧化功能及膳食来源抗氧化物质在体内的生物转化，故本申请在前期研究基础上提出"GSTM1/GSTT1基因多态性、富含黄酮类物质膳食摄入与AD之间可能存在交互作用"的假说。本研究采用人群病例对照研究、随访研究、动物及细胞实验并结合血清生理学、分子生物学等手段，从人群、动物、细胞多层次、多角度来验证假说，以明确GSTM1/GSTT1基因多态性、富含黄酮类物质膳食摄入与AD的关系，为 AD易感人群的筛选、临床预警及制定基于遗传背景的预防AD膳食指导方案提供科学依据。

Oxidative damage occurs early in the pathogenesis of AD, and it represents a potential therapeutic target for slowing the onset and progression of AD. As a result, the intake of antioxidants from diet is a feasible method to prevent AD. Our previous work indicated that flavonoids can prevent Aβ-induced learning and memory damage in vivo and neuron cells oxidative damgage in vitro. This study is a continue work of our previous project from the National Nature Scientific Foundation: "The effect of GSTM1/GSTT1 gene polymorphism on the response of health subjcets to flavonoid-rich dietary intervention". GSTM1/GSTT1 mainly contribute to body antioxidant capacity. And the polymorphisms of GSTM1/GSTT1 gene,caused by gene deletion,might affect body antioxidant capacity, and be related to a greater exposure to oxidative stress of an individual with unfavorable genotype. GST also invovled in the bitransformation of diet derived antioxidants. Therefore, the polymorphism of GSTM1/GSTT1 gene probably influence the antioxidants efficacy of dietary antioxidants. Base on our previous results, we proposed the interaction between flavonoid-rich diet intake and GSTM1/GSTT1 gene polymorphism in the development of AD. In the present study, we combined the methods of population case-control study, cohort study, animal experiment,in vitro cell culture, serophysiology and molecular biology techniques to explore the association of GSTM1/GSTT1 gene polymorphism and dietary flavonoids intake with AD. The results of the present study can help with the identification of sub-groups that present susceptibility to the development of AD. Also,understanding the relationship between GSTM1/GSTT1 gene polymorphism and flavonoid-rich diet intake in AD. And, the study may also provide genetic-based evidence for composing guide strategies for more successful intervention trials to prevent AD.