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Blockage of in vivo Aβ42 production, i.e., using antisense oligonucleotides to genes of key proteins involved in the production of Aβ42, leads to significant diminution of oxidative damage to brain, a conclusion that strengthens the notion that Aβ42 oligomer-associated oxidative damage and subsequent neurotoxicity is a fundamental process in mouse models of AD and MCI brains
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