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Under pathological conditions, FUNDC1 persists in a phosphorylated state that specifically impedes its molecular interaction with the autophagosomal marker protein LC3-II, consequently suppressing mitophagy initiation and ultimately inducing neuronal dysfunction ( Mitochondrial fragmentation has also been demonstrated in AD patients and model animals

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Children with inflammatory bowel diseases (IBDs) had increased GPx activity and GSH content compared with control children [72]