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They found that an imbalance of SAMe and SAH resulting from these vitamin deficiencies was associated with changes in methylation pattern of PSEN1 and BACE with consequent increases in PS1 and BACE levels, contributing to neurotoxic A deposition [6]

This oxidative stress can lead to cellular damage and inflammation, contributing to the overall toxic effects observed

While the dithiol mechanism for EcGrx1 and EcRNR or EcPR can be explained by specific protein-protein interactions (Fig