许多临床实践及实验研究表明，三焦针法治疗AD具有肯定的疗效。前期基础实验以SAMP8老化鼠作为研究对象，表明了该针刺方法能够改善老化鼠认知功能障碍，并抑制细胞凋亡及神经元的丢失。然该针刺方法如何抑制细胞凋亡及神经元丢失的内在机制的研究尚未清晰。最新的研究显示Aβ1-42作为痴呆主要的神经毒性因子，通过激活细胞内PI3K/PDK/PKC/Rac1信号通路诱导细胞凋亡。基于此，我们提出针刺抑制细胞凋亡改善认知功能可能是对该信号转导通路调控的假说。为了证实这一假说，本课题拟应用特异性抑制剂分别阻断PI3K/PDK1、nPKC、Rac1的表达，建立信号通路阻断模型，再分别从神经行为学和形态学上，利用病理学、免疫学、分子生物学等技术，探讨针刺对信号分子阻断前后的干预效应。本项目研究将深化针刺抗脑衰老机理的认识，为针刺应用于AD的防治提供新的理论依据。

Many clinical practice and experimental research show that the SanJiao (triple energizer) acupuncture treatment of AD have certain curative effect. Previous basic experiment in SAMP8 mice, proved that the acupuncture can improve cognitive dysfunction and inhibit cell apoptosis and neuron loss. But the study of the internal mechanism of acupuncture inhibiting cell apoptosis and neuron loss has not yet clear. The latest research shows that A beta 1-42 as dementia main nerve toxicity factor, by activating PI3K/PDK/PKC in the cell/Rac1 signaling pathways induced apoptosis. Based on this, we propose the hypothesis that acupuncture inhibited cell apoptosis may improve cognitive function by regulating the signal transduction pathway. To test this hypothesis, this project applicated specific inhibitors to block the expression of PI3K/PDK1, nPKC, Rac1, in ordor to set up signaling pathway block model, then respectively from neurological behavior and morphology, applying pathology, immunology and molecular biology technology, to analyse intervention effect of acupuncture on signal molecules before and after block. This research will deepen the understanding of mechanism of resisting brain aging by acupuncture, and provide a new theoretical basis for the prevention and treatment of acupuncture used in AD.