Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory impairment and progressive cognitive decline. Its core pathological mechanisms include β-amyloid deposition, abnormal tau phosphorylation, neuroinflammation, and decreased levels of neurotrophic factors. In recent years, the deficiency of neurotrophic factors has been recognized as a key driver of impaired neuronal survival and synaptic dysfunction. Consequently, restoring or enhancing neurotrophic factor signaling has emerged as a major therapeutic target for AD. As a traditional medicinal plant, ginseng exhibits multi-targeted, multi-level neuroprotective effects. Its active components—including ginsenosides, ginseng polysaccharides, and ginseng proteins—have been demonstrated to promote neuronal survival, inhibit apoptosis, and enhance synaptic plasticity by upregulating signaling pathways such as BDNF/TrkB and NGF/TrkA. Additionally, ginseng suppresses inflammatory responses and oxidative stress, thereby indirectly correcting neurotrophic factor imbalances and demonstrating significant neuroprotective potential. This review summarizes recent advances in ginseng's regulation of neurotrophic factor levels and signaling pathways, focusing on its molecular mechanisms for improving neuronal dysfunction and delaying AD progression. It also outlines future research strategies and prospects for clinical translation. In summary, ginseng's neuroprotective effects achieved through regulating the neurotrophic factor network offer a potential natural drug intervention strategy for AD treatment.
Huang et al. (Mon,) studied this question.