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Long-term radiofrequency electromagnetic fields exposure attenuates cognitive dysfunction in 5×FAD mice by regulating

Yeonghoon Son1, Hye-Jin Park1, Ye Ji Jeong1

  • 1Division of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, Korea.

Neural Regeneration Research
|June 7, 2023
PubMed
Summary

Long-term radiofrequency electromagnetic fields exposure in Alzheimer

Keywords:
5×FADAlzheimer’s diseaseCSF1Rlong term exposuremicroglial functionneuroinflammationradiofrequency electromagnetic fieldstherapeutic effect

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Area of Science:

  • Neuroscience
  • Biomedical Engineering
  • Alzheimer's Disease Research

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) deposition and glial activation.
  • Microglia play a crucial role in AD pathogenesis, with their activation contributing to neuroinflammation.
  • Previous studies indicated radiofrequency electromagnetic fields (RF-EMF) may reduce Aβ deposition and glial activation in 5×FAD mice.

Purpose of the Study:

  • To investigate if the therapeutic effects of RF-EMF in 5×FAD mice are mediated by regulating activated microglia.
  • To analyze microglial gene expression profiles and the presence of microglia in the brain following RF-EMF exposure.
  • To compare the effects of RF-EMF with a colony-stimulating factor 1 receptor (CSF1R) inhibitor on microglial activity.

Main Methods:

  • 5×FAD mice were exposed to 1950 MHz RF-EMF (5 W/kg) for 6 months.
  • Behavioral tests (object recognition, Y-maze) and molecular/histopathological analyses were performed.
  • Gene expression analysis of microglial markers (Iba1, CSF1R) and related pathways was conducted, comparing RF-EMF and CSF1R inhibitor (PLX3397) groups.

Main Results:

  • Six months of RF-EMF exposure ameliorated cognitive impairment and reduced Aβ deposition in 5×FAD mice.
  • RF-EMF exposure significantly reduced the expression of Iba1 and CSF1R in the hippocampus.
  • Both RF-EMF and PLX3397 suppressed genes associated with microgliosis (Csf1r, CD68, Ccl6) and pro-inflammatory interleukin-1β, as well as microglial function genes (Trem2, Fcgr1a, Ctss, Spi1).

Conclusions:

  • Long-term RF-EMF exposure effectively ameliorates Aβ pathology and cognitive deficits in a mouse model of Alzheimer's disease.
  • The therapeutic effects are linked to the suppression of amyloid-beta deposition-induced microgliosis.
  • RF-EMF acts by targeting the CSF1R pathway, a key regulator of microglial activation and proliferation.