PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration

Area of Science:

• Neuroscience
• Biomedical Engineering

Background:

• Alzheimer's disease (AD) involves cognitive decline, neuronal loss, oxidative stress, and mitochondrial dysfunction.
• Current AD therapies have limited efficacy and adverse effects.
• Pulsed electromagnetic fields (PEMFs) offer a non-invasive approach with potential therapeutic benefits.

Purpose of the Study:

• To investigate the neuroprotective potential of PEMFs in cellular models of AD.
• To determine PEMF effects on oxidative stress and mitochondrial function in AD-relevant conditions.

Main Methods:

• Utilized NGF-differentiated PC12 cells exposed to hydrogen peroxide (H₂O₂) or amyloid-β peptide (Aβ).
• Assessed cell viability, reactive oxygen species (ROS) production, catalase activity, and mitochondrial membrane potential.
• Measured caspase-3 activation, ERK phosphorylation, cAMP levels, CREB phosphorylation, and BDNF expression.

Main Results:

• PEMF treatment significantly improved cell viability and reduced cytotoxicity induced by H₂O₂ and Aβ.
• PEMFs restored catalase activity, decreased ROS production, and preserved mitochondrial membrane potential.
• PEMFs inhibited ERK phosphorylation, increased cAMP levels, enhanced CREB phosphorylation, and boosted BDNF expression.

Conclusions:

• PEMFs demonstrate significant neuroprotective effects against oxidative and amyloidogenic stress in cellular AD models.
• PEMF therapy modulates critical pathways involved in neuronal survival, plasticity, and stress response.
• PEMFs represent a promising non-invasive therapeutic strategy for Alzheimer's disease.