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Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating
Mengqing Li1, Qinyao Yu2, Umer Anayyat1
1Shenzhen University School of Basic Medical Sciences, Shenzhen, 518055, Guangdong, China.
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.
Insights
Rotating magnetic field (RMF) therapy improved memory and cognitive deficits in an Alzheimer's disease (AD) mouse model. RMF treatment reduced neuroinflammation by shifting microglia from M1 to M2 states, offering potential AD therapeutic applications.
Area of Science:
- Neuroscience
- Biomedical Engineering
- Neurodegenerative Diseases
Background:
- Neuroinflammation, driven by activated microglia, is central to Alzheimer's disease (AD) pathogenesis.
- Microglial activation involves pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes, influencing disease progression.
- Existing AD treatments have limitations, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the therapeutic potential of non-invasive rotating magnetic field (RMF) therapy.
- To evaluate RMF's effects on cognitive and memory impairments in a sporadic AD mouse model.
- To elucidate the underlying mechanisms of RMF action, including microglial polarization and signaling pathways.
Main Methods:
- A sporadic Alzheimer's disease (AD) mouse model was established using aluminum chloride (AlCl3) and D-galactose.
- Mice were treated with a rotating magnetic field (RMF) at 0.2T and 4Hz.
- Cognitive function, neuropathology (amyloid-beta deposition, hippocampal morphology, neuronal loss), neuroinflammation, microglial polarization (M1/M2), and signaling pathways (NF-κB/MAPK) were assessed. In vitro studies used cultured BV2 cells.
Main Results:
- RMF treatment significantly improved cognitive and memory impairments in AD mice.
- RMF reduced amyloid-beta deposition, mitigated hippocampal damage, prevented synaptic and neuronal loss, and decreased apoptosis.
- RMF ameliorated neuroinflammation by promoting M1 to M2 microglial polarization and inhibiting the NF-κB/MAPK pathway, also reducing brain aluminum deposition. In vitro, RMF enhanced amyloid phagocytosis and M1-M2 polarization in BV2 cells.
Conclusions:
- Rotating magnetic field (RMF) therapy demonstrates significant therapeutic benefits for cognitive and memory deficits in a sporadic AD model.
- RMF exerts its effects by modulating microglial polarization towards an anti-inflammatory M2 phenotype via inhibition of the NF-κB/MAPK signaling pathway.
- RMF represents a promising non-invasive therapeutic strategy for Alzheimer's disease treatment.
