Abstract：
Neuroinflammation, triggered by aberrantly activated microglia, is widely recognized as a key contributor to the initiation and progression of Alzheimer\'s disease (AD). Microglial activation in the central nervous system (CNS) can be classified into two distinct phenotypes: the pro-inflammatory M1 phenotype and the anti-inflammatory M2 phenotype. In this study, we investigated the effects of a non-invasive rotating magnetic field (RMF) (0.2T, 4Hz) on cognitive and memory impairments in a sporadic AD model of female Kunming mice induced by AlCl3 and D-gal. Our findings revealed significant improvements in cognitive and memory impairments following RMF treatment. Furthermore, RMF treatment led to reduced amyloid-beta (Aβ) deposition, mitigated damage to hippocampal morphology, prevented synaptic and neuronal loss, and alleviated cell apoptosis in the hippocampus and cortex of AD mice. Notably, RMF treatment ameliorated neuroinflammation, facilitated the transition of microglial polarization from M1 to M2, and inhibited the NF-кB/MAPK pathway. Additionally, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice. In cellular experiments, RMF promoted the M1-M2 polarization transition and enhanced amyloid phagocytosis in cultured BV2 cells while inhibiting the TLR4/NF-кB/MAPK pathway. Collectively, these results demonstrate that RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway. These findings suggest the promising therapeutic applications of RMF in the clinical treatment of AD.
摘要：
神经炎症,由异常激活的小胶质细胞引发，被广泛认为是阿尔茨海默病（AD）的发生和发展的关键因素。中枢神经系统（CNS）中的小胶质细胞活化可分为两种不同的表型：促炎M1表型和抗炎M2表型。在这项研究中,我们研究了非侵入性旋转磁场(RMF)(0.2T，4Hz）对AlCl3和D-gal诱导的雌性昆明小鼠散发性AD模型中的认知和记忆障碍。我们的发现揭示了RMF治疗后认知和记忆障碍的显着改善。此外，RMF治疗导致淀粉样β（Aβ）沉积减少，减轻对海马形态的损伤，防止突触和神经元的损失，减轻AD小鼠海马和皮质的细胞凋亡。值得注意的是,RMF治疗改善了神经炎症，促进了小胶质细胞极化从M1向M2的转变，并抑制了NF-κB/MAPK通路。此外,RMF处理导致AD小鼠脑中铝沉积减少。在细胞实验中,RMF促进培养的BV2细胞的M1-M2极化转变并增强淀粉样蛋白吞噬作用，同时抑制TLR4/NF-κB/MAPK通路。总的来说，这些结果表明，RMF可以改善零星AD模型中的记忆和认知障碍，可能通过抑制NF-κB/MAPK信号通路促进小胶质细胞极化的M1到M2转换。这些发现表明RMF在AD的临床治疗中的有希望的治疗应用。
