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In a previous study we have already experimentally demonstrated that a peripheral KA binding site exists in TyrBm 22

P = 0.10) per one standard deviation of genetically elevated GGT [75] , indicating no causality in the association between GGT and the risk for Alzheimers disease

A corresponding role for ferroptosis in human ASCVD is also supported by a genetic analysis of human coronary artery plaques which demonstrated a significant positive association between ferroptosis-related gene expression and ASCVD status 80,81

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