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

2023 · Benefit · Low evidence

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BenefitLow evidencePaper 384

Study snapshot

Publicationmanual · 2023

Study typeanimal

Reported directionBenefit

Evidence ratingLow

Abstract

Long-term radiofrequency electromagnetic fields exposure attenuates cognitive dysfunction in 5×FAD mice by regulating microglial function Son Y, Park HJ, Jeong YJ, Choi HD, Kim N, Lee HJ. Long-term radiofrequency electromagnetic fields exposure attenuates cognitive dysfunction in 5×FAD mice by regulating microglial function. Neural Regen Res. 2023 Nov;18(11):2497-2503. doi: 10.4103/1673-5374.371379. Abstract We have previously found that long-term effects of exposure to radiofrequency electromagnetic fields in 5×FAD mice with severe late-stage Alzheimer's disease reduced both amyloid-β deposition and glial activation, including microglia. To examine whether this therapeutic effect is due to the regulation of activated microglia, we analyzed microglial gene expression profiles and the existence of microglia in the brain in this study. 5×FAD mice at the age of 1.5 months were assigned to sham- and radiofrequency electromagnetic fields-exposed groups and then animals were exposed to 1950 MHz radiofrequency electromagnetic fields at a specific absorption rate of 5 W/kg for 2 hours/day and 5 days/week for 6 months. We conducted behavioral tests including the object recognition and Y-maze tests and molecular and histopathological analysis of amyloid precursor protein/amyloid-beta metabolism in brain tissue. We confirmed that radiofrequency electromagnetic field exposure for 6 months ameliorated cognitive impairment and amyloid-β deposition. The expression levels of Iba1 (pan-microglial marker) and colony-stimulating factor 1 receptor (CSF1R; regulates microglial proliferation) in the hippocampus in 5×FAD mice treated with radiofrequency electromagnetic fields were significantly reduced compared with those of the sham-exposed group. Subsequently, we analyzed the expression levels of genes related to microgliosis and microglial function in the radiofrequency electromagnetic fields-exposed group compared to those of a CSF1R inhibitor (PLX3397)-treated group. Both radiofrequency electromagnetic fields and PLX3397 suppressed the levels of genes related to microgliosis (Csf1r, CD68, and Ccl6) and pro-inflammatory cytokine interleukin-1β. Notably, the expression levels of genes related to microglial function, including Trem2, Fcgr1a, Ctss, and Spi1, were decreased after long-term radiofrequency electromagnetic field exposure, which was also observed in response to microglial suppression by PLX3397. These results showed that radiofrequency electromagnetic fields ameliorated amyloid-β pathology and cognitive impairment by suppressing amyloid-β deposition-induced microgliosis and their key regulator, CSF1R. Open access paper: ncbi.nlm.nih.gov

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typeanimal

Effect directionbenefit

Population5×FAD mice (Alzheimer’s disease model), starting at age 1.5 months

Sample sizeNot supplied

ExposureRF · 1950 MHz · 5 W/kg · 2 hours/day, 5 days/week for 6 months

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

In 5×FAD mice, 6 months of 1950 MHz RF-EMF exposure (SAR 5 W/kg) improved performance on behavioral tests and reduced amyloid-β deposition compared with sham exposure. RF-EMF exposure was associated with reduced hippocampal Iba1 and CSF1R levels and decreased expression of genes related to microgliosis and IL-1β; microglial function-related genes were also decreased, similar to effects seen with the CSF1R inhibitor PLX3397.

Outcomes measured

Cognitive function (object recognition test, Y-maze)
Amyloid-β deposition/pathology
Microglial markers (Iba1)
CSF1R expression
Gene expression related to microgliosis (Csf1r, CD68, Ccl6)
Pro-inflammatory cytokine IL-1β
Microglial function-related genes (Trem2, Fcgr1a, Ctss, Spi1)

Limitations

Sample size not reported in the provided abstract/metadata
Animal model study; generalizability to humans not addressed in the provided abstract
Exposure source/setup details not provided in the provided abstract

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": 1950,
    "sar_wkg": 5,
    "duration": "2 hours/day, 5 days/week for 6 months"
  },
  "population": "5×FAD mice (Alzheimer’s disease model), starting at age 1.5 months",
  "sample_size": null,
  "outcomes": [
    "Cognitive function (object recognition test, Y-maze)",
    "Amyloid-β deposition/pathology",
    "Microglial markers (Iba1)",
    "CSF1R expression",
    "Gene expression related to microgliosis (Csf1r, CD68, Ccl6)",
    "Pro-inflammatory cytokine IL-1β",
    "Microglial function-related genes (Trem2, Fcgr1a, Ctss, Spi1)"
  ],
  "main_findings": "In 5×FAD mice, 6 months of 1950 MHz RF-EMF exposure (SAR 5 W/kg) improved performance on behavioral tests and reduced amyloid-β deposition compared with sham exposure. RF-EMF exposure was associated with reduced hippocampal Iba1 and CSF1R levels and decreased expression of genes related to microgliosis and IL-1β; microglial function-related genes were also decreased, similar to effects seen with the CSF1R inhibitor PLX3397.",
  "effect_direction": "benefit",
  "limitations": [
    "Sample size not reported in the provided abstract/metadata",
    "Animal model study; generalizability to humans not addressed in the provided abstract",
    "Exposure source/setup details not provided in the provided abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "radiofrequency electromagnetic fields",
    "RF-EMF",
    "1950 MHz",
    "specific absorption rate",
    "SAR 5 W/kg",
    "5×FAD",
    "Alzheimer’s disease model",
    "cognition",
    "amyloid-β",
    "microglia",
    "microgliosis",
    "CSF1R",
    "Iba1",
    "PLX3397"
  ],
  "suggested_hubs": [
    {
      "slug": "who-icnirp",
      "weight": 0.2,
      "reason": "Uses SAR-based RF exposure parameters relevant to RF safety frameworks, though no policy discussion is provided."
    }
  ]
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.4103/1673-5374.371379
PubMed: Not supplied

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