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It has been found that mutations in the amyloid protein precursor ( APP ), presenilin-1 ( PSEN1 ), and presenilin-2 ( PSEN2 ) genes are associated with autosomal dominant early-onset familial AD, while apolipoprotein E4 ( APOE4 ) represents the most significant genetic risk factor for late-onset sporadic AD, contributing to the deposition of A peptides and hyperphosphorylated tau proteins (Giau et al., 2019

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Further consistent with this mechanism, Gem pretreatment did not suppress ferroptosis induced by the direct GPX4 inhibitor ML162, whose ability to induce ferroptosis is independent of intracellular GSH pools (Yang et al, 2014) (Fig 4F)