BACKGROUND Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive loss of cognitive abilities and memory leading to dementia. Electroacupuncture (EA) is a complementary alternative medicine approach, applying an electrical current to acupuncture points. In clinical and animal studies, EA causes cognitive improvements in AD and vascular dementia. However, EA-induced changes in cognition and microglia-mediated amyloid β (Aβ) degradation have not been determined yet in AD animals. Therefore, this study investigated the EA-induced molecular mechanisms causing cognitive improvement and anti-inflammatory activity in five familial mutation (5XFAD) mice, an animal model of AD. METHODS 5XFAD mice were bilaterally treated with EA at the Taegye (KI3) acupoints three times per week for 2 weeks. To evaluate the effects of EA treatment on cognitive functions, novel object recognition and Y-maze tests were performed with non-Tg, 5XFAD (Tg), and EA-treated 5XFAD (Tg + KI3) mice. To examine the molecular mechanisms underlying EA effects, western blots, immunohistochemistry, and micro-positron emission tomography scans were performed. Furthermore, we studied synapse ultrastructures with transmission electron microscopy and used electrophysiology to investigate EA effects on synaptic plasticity in 5XFAD mice. RESULTS EA treatment significantly improved working memory and synaptic plasticity, alleviated neuroinflammation, and reduced ultrastructural degradation of synapses via upregulation of synaptophysin and postsynaptic density-95 protein in 5XFAD mice. Furthermore, microglia-mediated Aβ deposition was reduced after EA treatment and coincided with a reduction in amyloid precursor protein. CONCLUSIONS Our findings demonstrate that EA treatment ameliorates cognitive impairment via inhibition of synaptic degeneration and neuroinflammation in a mouse model of AD.

中文翻译：

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在阿尔茨海默氏病动物模型中，电针可通过抗神经炎症作用减轻认知障碍。

背景技术阿尔茨海默氏病（AD）是一种神经退行性疾病，其特征在于认知能力和记忆的进行性丧失导致痴呆。电针（EA）是一种替代性的替代医学方法，向穴位施加电流。在临床和动物研究中，EA导致AD和血管性痴呆的认知改善。但是，尚未在AD动物中确定EA诱导的认知变化和小胶质细胞介导的淀粉样β（Aβ）降解。因此，本研究调查了五种家族性AD动物模型（5XFAD）小鼠中EA诱导的引起认知改善和抗炎活性的分子机制。方法每周3次在Taegye（KI3）穴位对EA进行5XFAD小鼠双侧治疗，共2周。为了评估EA治疗对认知功能的影响，对非Tg，5XFAD（Tg）和EA治疗的5XFAD（Tg + KI3）小鼠进行了新颖的物体识别和Y迷宫测试。为了检查EA影响的分子机制，进行了蛋白质印迹，免疫组织化学和微正电子发射断层扫描。此外，我们用透射电子显微镜研究了突触的超微结构，并用电生理学研究了EA对5XFAD小鼠突触可塑性的影响。结果EA治疗可通过上调5XFAD小鼠的突触素和突触后密度95蛋白来显着改善工作记忆和突触可塑性，减轻神经炎症，并减少突触的超微结构降解。此外，小胶质细胞介导的Aβ沉积在EA处理后减少，并且与淀粉样蛋白前体蛋白的减少同时发生。结论我们的发现表明EA治疗可通过抑制AD小鼠模型中的突触变性和神经炎症来改善认知障碍。