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<p>Non‑invasive physical therapies such as radiofrequency electromagnetic fields (RF‑EMF) and pulsed magnetic fields (PMF) have been proposed as promising interventions for neuroinflammatory disorders. Bindal and colleagues recently reported that RF‑EMF and PMF attenuate LPS‑induced neuroinflammation in a rat model, attributing the effect to PI3K/AKT/HIF‑1α signalling. While the study addresses an important question, four methodological limitations warrant consideration: (i) the claimed non‑thermal mechanism is unsubstantiated without direct brain temperature measurement despite a 1&#xa0;°C temperature increase; (ii) pathway activation is inferred solely from mRNA data without protein‑level confirmation (p‑AKT/total‑AKT ratios); (iii) no dosimetric characterisation (SAR) is provided, contradicting ICNIRP guidelines; and (iv) the absence of a positive control leaves the clinical relevance unanchored. These considerations suggest that the evidence for non‑thermal neuroprotection via PI3K/AKT/HIF‑1α signalling is less robust than presented, and the findings are best viewed as hypothesis‑generating.</p>

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Correspondence: Radiofrequency and pulsed magnetic fields in LPS‑induced neuroinflammation: interpreting the evidence for PI3K/AKT/HIF‑1α‑mediated protection

  • 期刊论文

  • 发表日期：

    2026年7月25日

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  • Shumoos Aziz Fadhil,
  • Fatemeh Mortazavi Moghadam,
  • Umida Azzamova,
  • Shaxnosa Mamatova,
  • Xusniddin Ramazonov,
  • Vohid Samadov,
  • Arman Abroumand Gholami

摘要

Non‑invasive physical therapies such as radiofrequency electromagnetic fields (RF‑EMF) and pulsed magnetic fields (PMF) have been proposed as promising interventions for neuroinflammatory disorders. Bindal and colleagues recently reported that RF‑EMF and PMF attenuate LPS‑induced neuroinflammation in a rat model, attributing the effect to PI3K/AKT/HIF‑1α signalling. While the study addresses an important question, four methodological limitations warrant consideration: (i) the claimed non‑thermal mechanism is unsubstantiated without direct brain temperature measurement despite a 1 °C temperature increase; (ii) pathway activation is inferred solely from mRNA data without protein‑level confirmation (p‑AKT/total‑AKT ratios); (iii) no dosimetric characterisation (SAR) is provided, contradicting ICNIRP guidelines; and (iv) the absence of a positive control leaves the clinical relevance unanchored. These considerations suggest that the evidence for non‑thermal neuroprotection via PI3K/AKT/HIF‑1α signalling is less robust than presented, and the findings are best viewed as hypothesis‑generating.