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Additionally, miR-9 contributes to AD pathogenesis by inducing ferroptosis through targeted inhibition of SLC7A11, thereby blocking GSH synthesis, and additionally participates in regulating NFTs formation (220)

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and patients with glutathione-S-transferase M1 (proinflammatory-cytokine producer macrophages) null and M1 and T1 (Type 1 helper CD4 + lymphocytes) double null polymorphisms had increased mortality suggesting that antioxidant therapy becomes fundamental for those patients (109)