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This cross-efficacy between drugs used for the two conditions may indirectly support the hypothesis of a shared pathogenesis

Because H 2 O 2 increases Nrf2 binding to DNA, a potential neuroprotective mechanism is that transient elevation of H 2 O 2 and altered redox states from the KD serve to activate Nrf2 leading to induction of antioxidation pathways (60)

(2019) in serum following a PEM challenge

especially at the active site, the FAD-binding region, and the pyridine nucleotide binding region.[8] Lipoamide dehydrogenase (E3) is the terminal enzyme in both the pyruvate and a-ketoglutarate dehydrogenase complexes