APP and Alzheimer disease: <i>In vitro</i>, salidroside attenuated reactive oxygen species (ROS) generation, inhibited neuronal apoptosis, and suppressed Aβ production, demonstrating broad neuroprotective effects relevant to AD pathology.<h4>Conclusion</h4>Our results suggest that salidroside may alleviate mitochondrial dysfunction and reduce mitochondrial protein aggregation by modulating APP processing, promoting sAPPα production while decreasing β-CTF and Aβ levels.