突触丢失和Tau病理是阿尔茨海默病（AD）的重要病理征，与认知功能下降更相关。Tau病理可导致突触丢失，但具体机制尚不明确。最新研究表明，发育阶段，补体C1q依赖的小胶质细胞（Microglia）突触修剪功能过度激活在Tau病理导致的突触丢失中起重要作用。我们前期研究表明，电针能够改善AD模型小鼠的突触丢失和减轻Tau病理。因此，我们提出如下假说，电针通过抑制Tau/C1q/Microglia途径改善AD的突触丢失。为验证上述假说，本课题拟在前期基础上，以SAMP8小鼠为AD动物模型，体外实验运用电针血清干预，应用电镜、免疫荧光、流式细胞术、Western blot、Real-time PCR和RNA干扰等技术，从体内及体外实验深入研究Tau/C1q/Microglia途径在电针改善AD突触丢失中的作用，以期阐明电针改善AD突触丢失的机制，为临床电针防治AD提供新的理论基础。

Synapse loss and Tau pathology are hallmarks of Alzheimer’s disease (AD) and are currently the best correlate to cognitive decline in AD, but how Tau pathology causes synapse loss is unclear. Recent studies have revealed that microglia is involved in synapse pruning during development via a complement C1q-dependent manner. C1q-dependent microglial phagocytosis of synapses is re-activated and plays an important role in synaptic loss associated with Tau. Our previous studies showed that Electroacupuncture（EA）alleviated synaptic loss and Tau pathology in AD animal model. Thus, we hypothesized that EA reduces the extent of synaptic loss in AD via the inhibition of Tau/C1q/Microglia pathway. To test the hypothesis, SAMP8 mice, acupuncture serum, Electron microscope, immunofluorescence, flow cytometry, western blot, Real-time PCR and RNA interference are employed in this study. We investigate the role of Tau/C1q/Microglia pathway in EA alleviating synaptic loss in vivo and in vitro, which may contribute to clarify the mechanisms underlying EA alleviating synaptic loss in AD, and provide the new theoretical basis for prevention and treatment of AD by EA.