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This article begins with an overview of basic pathological mechanisms and offers a comprehensive overview of relevant therapeutic approaches and future development directions, aiming to facilitate the transition of the field from traditional generalized therapies to personalized precision medicine and to bridge the long-standing gap between basic research and clinical practice.

Performing positive pixel density scoring on immunohistochemically stained post-mortem Brodmann Area 17 sections revealed that the progression of AD pathology was accompanied by decreased expression of nuclear receptor co-activator 4 and glutathione peroxidase 4 in the grey matter

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HepG2 cells exhibited higher catalase activity than HeLa cells, and inhibiting catalase activity by using 3-aminotriazole (3-AT, a specific inhibition of catalase) or catalase siRNA remarkably reduced the resistance of HepG2 cells to ROS, demonstrating the key roles of catalase for the strong resistance of HepG2 cells to ROS

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