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Blockage of in vivo A42 production, i.e., using antisense oligonucleotides to genes of key proteins involved in the production of A42, leads to significant diminution of oxidative damage to brain, a conclusion that strengthens the notion that A42 oligomer-associated oxidative damage and subsequent neurotoxicity is a fundamental process in mouse models of AD and MCI brains

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FIGURE 3 3.5 Disease-gene network correlates hub OS-DEGs with multi-disease associations underlying cellular stress mechanisms The disease-gene association network highlights hub genes including GPx4, SOD1, SOD2, ATM, CAT, TP53, SNCA, FOS, G6PD, IL6, EDN1, HSPB1, and MPO as critical hubs involved in OS-related diseases (Figure 3C)