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1:20), and -1-antitrypsin (A1AT) mouse anti-human monoclonal antibody (cat

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Increasing evidence highlights ferroptosis as a pivotal contributor to the pathogenesis of NDDs (Table 1), suggesting that therapeutic targeting of ferroptosis may offer a promising strategy for the prevention and treatment of NDDs

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(2018) demonstrated that NAC treatment significantly reduced H 2 O 2 -induced tau phosphorylation at multiple sites, including Ser199, Ser202, Thr205, and Ser396 [29]