Abstract
Alzheimer's disease (AD) is a neurodegenerative pathology covering about 70% of all cases of dementia. It is associated with neuroinflammation and neuronal cell death, which are involved in disease progression. There is a lack of effective therapies, and halting this process represents a therapeutic challenge. Data in the literature suggest several neuroprotective effects of low-frequency, low-energy pulsed electromagnetic fields (PEMFs) on biological systems, and clinical studies report that PEMF stimulation is safe and well tolerated. The aim of this work is to investigate the effects of PEMF exposure on oxidative stress and cell death in in vitro-injured cellular models of neurons and microglia. SH-SY5Y cells were stimulated by hydrogen peroxide (H(2)O(2)) or amyloid-β (Aβ) peptide, and N9 microglial cells were activated with lipopolysaccharide (LPS) or Aβ peptide. Reactive oxygen production, mitochondrial integrity, and cell death modulation were investigated through 2',7'-dichlorodihydrofluorescein diacetate (H(2)DCFDA) and 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbo-cyanine iodide (JC-1) biochemical assays, fluorescence, and MTS experiments. Cells were exposed to PEMFs producing a pulsed signal with the following parameters: pulse duration of 1.3 ms and frequency of 75 Hz. The outcomes demonstrated that PEMFs defended SH-SY5Y cells against Aβ peptide- or H(2)O(2)-induced oxidative stress, mitochondrial damage, and cell death. Furthermore, in microglia activated by LPS or Aβ peptide, they reverted the reduction in mitochondrial potential, oxidative damage, and cell death. Overall, these findings imply that PEMFs influence the redox state of the cells by significantly boosting antioxidant levels in both injured microglia and neuronal in vitro cells mimicking in vitro AD.