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Other mechanisms of action are also known, such as the inhibition of phosphodiesterase, mobilization of intracellular calcium, and the antagonism of GABAa receptors at toxic levels of caffeine [13]

Both irradiation modalities affected purine metabolism and lysine degradation pathways in TM3 cells, suggesting that changes in ADP levels may serve as a key metabolic signature in the cellular response to RF-EMF exposure

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Oxidative stress, dysfunctional mitochondria, and neuroinflammation have all been suggested to play roles in the onset and progression of PD (Navarro and Boveris, 2009