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More specifically, when astrocytes became reactive they unleash the pathological effects of amyloid-beta on downstream tau phosphorylation and deposition, which very likely will lead to cognitive deterioration
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However, this study lacks clinical validation of the USP15/LGALS3/AKT/mTOR axis in lenvatinib-treated patient specimens, and the mechanistic details underlying USP15-driven AKT/mTOR activation remain unresolved [166]
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