Panax ginseng: A modulator of amyloid, tau pathology, and cognitive function in Alzheimer's disease

Alzheimer's disease (AD), the leading cause of dementia, is characterized by the presence of beta-amyloid (Aβ) plaques, tau hyperphosphorylation, and cognitive decline. Despite advancements in Aβ-targeting therapies, the multifaceted nature of AD underscores the need for complementary treatments. Panax ginseng, renowned for its cognitive-enhancing properties, has demonstrated potential in addressing AD pathology. This review systematically explores the therapeutic potential of P. ginseng and its bioactive ginsenosides, focusing on their effects on Aβ, tau proteins, and cognitive function. We summarize the findings from preclinical and clinical studies, highlighting neuroprotective mechanisms, such as the inhibition of Aβ production, enhanced Aβ clearance, and suppression of tau hyperphosphorylation. Research on P. ginseng and its bioactive ginsenosides has shown potential for improving cognitive function in AD models. Clinical studies further suggest its cognitive benefits in mild cognitive impairment, subjective memory impairment, and as adjunctive therapy in AD, with particularly pronounced effects in individuals lacking apolipoprotein ε4 allele. This review provides a comprehensive overview of the potential of P. ginseng as both a therapeutic and preventive agent for AD, highlighting the scientific basis for further exploration of P. ginseng-derived compounds to optimize their efficacy and clinical application.