Department of Rehabilitation, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Department of Tuina, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518000, China.
Curr Med Sci. 2024 Oct;44(5):987-1000. doi: 10.1007/s11596-024-2908-9. Epub 2024 Jul 11.
Alzheimer's disease (AD) has become a significant global concern, but effective drugs able to slow down AD progression is still lacked. Electroacupuncture (EA) has been demonstrated to ameliorate cognitive impairment in individuals with AD. However, the underlying mechanisms remains poorly understood. This study aimed at examining the neuroprotective properties of EA and its potential mechanism of action against AD.
APP/PS1 transgenic mice were employed to evaluate the protective effects of EA on Shenshu (BL 23) and Baihui (GV 20). Chemogenetic manipulation was used to activate or inhibit serotonergic neurons within the dorsal raphe nucleus (DRN). Learning and memory abilities were assessed by the novel object recognition and Morris water maze tests. Golgi staining, western blot, and immunostaining were utilized to determine EA-induced neuroprotection.
EA at Shenshu (BL 23) and Baihui (GV 20) effectively ameliorated learning and memory impairments in APP/PS1 mice. EA attenuated dendritic spine loss, increased the expression levels of PSD95, synaptophysin, and brain-derived neurotrophic factor in hippocampus. Activation of serotonergic neurons within the DRN can ameliorate cognitive deficits in AD by activating glutamatergic neurons mediated by 5-HT. Chemogenetic inhibition of serotonergic neurons in the DRN reversed the effects of EA on synaptic plasticity and memory.
EA can alleviate cognitive dysfunction in APP/PS1 mice by activating serotonergic neurons in the DRN. Further study is necessary to better understand how the serotonergic neurons-related neural circuits involves in EA-induced memory improvement in AD.
阿尔茨海默病（AD）已成为全球关注的重大问题，但仍缺乏能够减缓 AD 进展的有效药物。电针（EA）已被证明可改善 AD 患者的认知障碍。然而，其潜在的作用机制仍知之甚少。本研究旨在探讨 EA 的神经保护作用及其对 AD 的潜在作用机制。
采用 APP/PS1 转基因小鼠评估 EA 对肾俞（BL 23）和百会（GV 20）的保护作用。化学遗传操作用于激活或抑制中缝背核（DRN）内的 5-羟色胺能神经元。通过新物体识别和 Morris 水迷宫测试评估学习和记忆能力。利用高尔基染色、western blot 和免疫染色来确定 EA 诱导的神经保护作用。
EA 在肾俞（BL 23）和百会（GV 20）可有效改善 APP/PS1 小鼠的学习和记忆障碍。EA 可减轻树突棘丢失，增加海马 PSD95、突触小体蛋白和脑源性神经营养因子的表达水平。DRN 内 5-羟色胺能神经元的激活可通过 5-HT 激活谷氨酸能神经元来改善 AD 的认知障碍。DRN 中 5-羟色胺能神经元的化学遗传抑制可逆转 EA 对突触可塑性和记忆的影响。
EA 通过激活 DRN 中的 5-羟色胺能神经元可减轻 APP/PS1 小鼠的认知功能障碍。需要进一步研究以更好地了解与 5-羟色胺能神经元相关的神经回路如何参与 EA 诱导的 AD 记忆改善。
