人口老龄化是目前社会的主要问题之一，而衰老是老年性疾病尤其老年痴呆发生的主要原因。G蛋白偶联雌激素受体(GPR30)是新近发现的一种膜性雌激素受体，在衰老、认知功能的发挥中有关键作用。人参具有类雌激素特性，能延缓衰老和促认知等功能，但是人参作用的本质不清楚。人参皂苷类是人参主要的活性成分，我们发现人参皂苷Rg1具有促进老年小鼠海马突触结构可塑性，改善学习记忆功能。结合TrkB通路在记忆过程发挥关键的作用，本项目提出人参皂苷Rg1促进GPR30调节TrkB通路促进老年小鼠学习记忆的假设。为证实该假设，本项目拟从细胞分子、神经通路、行为功能层面阐明人参皂苷Rg1通过促进GPR30改善老年小鼠突触结构可塑性、海马神经通路和学习记忆，探索人参皂苷Rg1经由GPR30调节CDK5促进TrkB信号通路可能性的机制。本项目的研究为揭示衰老发展机制，还原人参益智的本质提供重要参考。

Aging is now a primary social issue in China and supposed as the culprit of neurodegenerative diseases, especially in Alzheimer’s disease (AD). G protein-coupled estrogen (GPR30) is one recently identified membrane estrogen and performs critical roles in aging and learning and memory. Ginseng possesses estrogen-like activity and has the abilities to postpone aging and enhance memory. However, the mechanisms are not well disclosed. Ginsenosides are the active components in ginseng and we previously reported that ginsenoside Rg1 facilitated spinogenesis, synaptic plasticity and memory in aging mice. Considering the prominent roles of TrkB performed in memory formation, we hypothesized that ginsenoside Rg1 promoted GPR30 to enhance hippocampal synaptic circuit and memory in aging mice through regulating TrkB. From molecular level to circuit and behavior, we will elucidate the protective effects of ginsenoside Rg1 on hippocampal synaptic circuit and memory in aging mice through promoting GPR30 activity. As the mechanisms, we will investigate the potential regulation of TrkB by GPR30 activation through CDK5 phosphorylation. This study will provide novel explanations for the development of aging and emphasize GPR30 as a potential target for ginsenosides in memory improving.