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Given that overexpression of dual-specificity tyrosine phosphorylation-regulated kinase 1 A (DYRK1A) may influence the initial progression of AD through mechanisms including the hyperphosphorylation of pathologically relevant substrates such as tau, APP, PS1, regulation of axonal transport of APP, and participation in the selective splicing of tau pre-mRNA, 500,501,502 the compound dp-FINDY ( 37 ) effectively targets the spatial dynamic changes in the ATP-binding site between the DYRK1A folding intermediate and the folded state, specifically acting on the folding intermediate
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Similarly, SOD1 overexpression has been reported to reduce ROS generation and inhibit viral replication and the inflammatory response 27
