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On the other hand, inflammatory conditions may increase drug-protein binding due to acute phase proteins such as -1-acid glycoprotein are produced [23, 32]

Key mechanisms include their high susceptibility to iron-dependent cell death, polarization toward a pro-inflammatory state under iron overload, and genetic regulation by factors such as LRRK2 and DJ-1

The limited controlled trial data showed modest effects at best, which is a long way from establishing clinical usefulness

I think I'm paraphrasing him for sure, but I think that's accurate