非编码微小RNA的表观遗传及转录调控在AD复杂发病机制中发挥了重要作用。我们此前发现，AD小鼠脑内miR-148a-3p的表达降低与神经炎症密切相关，并受到靶基因RAGE及关联通路分子α7nAChR的反向特异性调控。近期又发现，中药香青兰提取物防治AD的作用与其活性单体调节miR-148a-3p/RAGE信号通路显著相关。但miR-148a-3p通过靶基因及关联信号途径减缓AD神经炎症的时序性与特异性机制及香青兰的干预位点均不明确。本课题拟以miR-148a-3p作为调节RAGE/α7nAChR通路的新靶标，对炎症信号分子间相互作用机制进行基因水平的追溯研究。综合利用生物信息学、分子生物学、蛋白通路芯片等技术，从基因功能、病理通路、药物作用等方面，探究miR-148a-3p经由RAGE/α7nAChR在AD炎症损伤中形成的串联、级联或反馈性的多向调控机制，阐释香青兰抗炎防治AD的作用机理。

The pathophysiology of AD is very complicated, and the no-coding genes and other epigenetic and transcription regulated element may play an important role. Based on the previous research, we found that miR-148a-3p is down-regulated in AD mouse brain, which is negative connected with neuroinflammatory reaction. We suggested that the target gene of miR-148a-3p is RAGE, and that miR-148a-3p can be specifically regulated by inflammatory signal pathway proteins, such as RAGE and α7nAChR. Recently, we found that the extracts from Dracocephalum Moldavica L could prevent AD and the active compounds from Dracocephalum Moldavica L have an important influence on miR-148a-3p/RAGE signal pathway. Up to now, the mechanism of miR-148a-3p regulating RAGE/α7nAChR signal pathway and reducing neuroinflammatory reaction, or the targeted gene of Dracocephalum Moldavica L has not been cleared yet. Herein, our research considers miR-148a-3p as the new target of RAGE/α7nAChR signaling pathway and studies the genetic level of the interaction mechanisms between the molecules in inflammatory signaling pathways. We will comprehensively use the methods and techniques of bioinformatics, molecular biology and protein chip technology. And we will investigate the function and pathology of miR-148a-3p in three aspects of gene function, pathological pathways and drug reaction. Finally, we will get to the aim of exploration of miR-148a-3p cascades or its feedback multidirectional mechanisms in AD inflammatory injury through RAGE/α7nAChR signal pathway, and then explain the mechanisms of Dracocephalum Moldavica L of preventing and treating AD based on the neuroinflammatory mechanism.