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Further, pharmacological inhibition of mitochondrial enzyme complexes results in decreased oxidative phosphorylation and seizure activity ( There are numerous indications that increased ROS production occurs across epilepsy models, as evidenced by oxidative damage and impaired redox status

There was a 2015 Phase I human trial registered to study safety and pharmacokinetics, but published results are conspicuously missing

Despite these assumptions, no direct evidence exist supporting bacterial or endotoxin transport through the paracellular pathway

Nystrm, E.J