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Candidate mechanisms include activation of Nrf2-dependent antioxidant programs, preservation of glutathione, inhibition of NADPH oxidases, and reduced inflammatory RONS production by microglia and macrophages [22,23,24,25,26]
Oral GHK-Cu offers convenience but delivers substantially less peptide to the bloodstream
Table 1 Riboflavin-responsive neurological disorders: mechanisms, dosing, outcomes, and evidence strength
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