乙酰基-11-酮基-β-乳香酸（AKBA）是传统药物乳香最主要的生物活性成分，广泛应用于心肌缺血、炎症性肠病和支气管哮喘等疾病的治疗。近年来AKBA的抗氧化神经保护作用日益受到关注。我们前期研究发现，AKBA可显著改善APPswe/PS1dE9转基因小鼠的空间学习和记忆能力，并增加其皮质和海马组织中Nrf2的蛋白含量。据此推论，AKBA可能通过激活Nrf2/ARE信号通路，增强神经元的抗氧化能力，阻断阿尔茨海默病（AD）的病理进程，修复突触活动和神经传递，从而实现治疗AD的作用。本课题拟通过动物行为学、组织形态学、神经电生理和分子生物学等方法，基于Nrf2/ARE信号途径，在动物、细胞和分子等层面探讨AKBA对AD认知功能障碍的改善及作用机制，以期揭示AD病变的发生和发展过程，并为研发AD治疗药物提供新的研究思路和作用靶点。

Acetyl-11-keto-β-boswellic acid (AKBA) is the most important bioactive component of traditional medicine frankincense and is widely used in the treatment of diseases such as myocardial ischemia, inflammatory bowel disease and bronchial asthma. In recent years, the antioxidant neuroprotective effect of AKBA has drawn increasing attention. Our previous study found that AKBA can significantly improve the spatial learning and memory ability and increase the protein content of Nrf2 in cortex and hippocampus of APPswe/PS1dE9 transgenic mice. It is concluded that AKBA may enhance neuronal antioxidant capacity, block the pathological process of Alzheimer’s disease (AD), and repair synaptic activity and neurotransmission by activating Nrf2/ARE signaling pathway. In this study, we aimed to explore the mechanism of AKBA on AD cognitive dysfunction improvement based on the Nrf2/ARE signaling pathway through animal behavioral, histomorphological, neural electrophysiological and molecular biological methods. This research project may reveal the occurrence and development of AD and provide new research ideas and targets for the AD treatment.