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Two principal mechanisms have been proposed: the classical transferrin-dependent pathway and the transcytosis model ( + is reduced to Fe + , exported into the cytosol by divalent metal transporter 1 (DMT1), and subsequently released across the abluminal membrane via ferroportin 1 (FPN1), followed by re-oxidation through ceruloplasmin before entering the brain parenchyma (172, 173)

When the ROS burden cannot be alleviated because of reduced or lack of sleep, the redox imbalance persists and causes cellular damage

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