Alzheimer’s disease (AD) is a chronic neurodegenerative disease that is characterized by the extracellular accumulation of β-amyloid (Aβ). Many studies have shown a close relationship between autophagy and the formation of Aβ. As AD develops and progresses, mitophagy diminishes insoluble Aβ, and mitochondrial dysfunction seems to be a determining factor in the pathogenesis of AD. In our previous study, we showed that β-asarone pharmacological effects in APP/PS1 transgenic mice, reducing Aβ expression. However, the specific mechanism of this effect remains unclear. In this study, AD model rats induced by intracerebroventricular injection of Aβ_1-42 were randomly divided into nine groups, and medical intervention was applied to the animals for 30 days. Subsequently, spatial learning and memory were evaluated by the water maze test. Bcl-2 levels in the hippocampus were determined by western blotting (WB). The protein expression of Aβ_1-42, Beclin-1, p62, PINK1, and Parkin was assessed by WB and immunohistochemistry (IHC). The data showed that after β-asarone treatment, the learning and memory of the AD rats were clearly improved compared with those of the model group. Moreover, β-asarone decreased Aβ_1-42, Bcl-2, and p62 levels but increased Beclin-1 levels compared with those in the model group. In addition, we treated a group of rats with CsA to inhibit mitophagy. β-Asarone increased PINK1 and Parkin expression compared with that in the model group. The results showed that β-asarone can improve the learning and memory of rats with Aβ_1-42-induced AD by effectively promoting PINK1-Parkin-mediated mitophagy. Taken together, these results suggest that β-asarone may have the capacity to become a pharmaceutical agent for the treatment of AD in the future.

阿尔茨海默病 (AD) 是一种慢性神经退行性疾病，其特征在于 β-淀粉样蛋白 (Aβ) 的细胞外积累。许多研究表明，自噬与 Aβ 的形成密切相关。随着 AD 的发展和进展，线粒体自噬减少不溶性 Aβ，线粒体功能障碍似乎是 AD 发病机制的决定性因素。在我们之前的研究中，我们发现 β-细辛醚在 APP/PS1 转基因小鼠中的药理作用降低了 Aβ 的表达。然而，这种效应的具体机制仍不清楚。_{本研究采用 Aβ 1-42}脑室内注射诱导的 AD 模型大鼠随机分为9组，对动物进行医疗干预30天。随后，通过水迷宫测试评估空间学习和记忆。通过蛋白质印迹（WB）测定海马中的Bcl-2水平。_{通过 WB 和免疫组织化学 (IHC) 评估 Aβ 1-42}、Beclin-1、p62、PINK1 和 Parkin的蛋白质表达。资料显示，经β-细辛醚治疗后，AD大鼠的学习记忆能力较模型组有明显改善。此外，β-细辛醚降低 Aβ _1-42、Bcl-2 和 p62 水平，但与模型组相比，Beclin-1 水平升高。此外，我们用 CsA 治疗了一组大鼠以抑制线粒体自噬。与模型组相比，β-细辛醚增加了 PINK1 和 Parkin 的表达。结果表明，β-细辛可以通过有效促进PINK1-Parkin介导的线粒体自噬来改善_{Aβ1-42诱导的AD大鼠的学习记忆能力。}综上所述，这些结果表明β-细辛醚将来可能有能力成为治疗AD的药剂。