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It is needed for neurotransmitter reuptake, endocytosis of SV, and presynaptic vesicles, let alone maintain the concentration gradients of ions across the membrane

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To further characterize these interactions, we constructed a molecular interaction network (Figure 7C) revealed three functionally interconnected modules: (Young et al., 1990) an oxidative stress module linking Gpx3 with glutathione metabolites, and ( Consistent with multi-omics findings, KEGG pathway analysis identified glutathione metabolism as the most significantly perturbed shared pathway (Figure 8A), exhibiting coordinated changes between upregulated antioxidant enzymes such as Gpx3 and Mgst1 alongside depleted glutathione derivatives, supporting redox imbalance as a key pathogenic feature

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