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Loss of redox flexibility compromises protein thiol regulation, redox-sensitive signaling pathways, and endothelial homeostasis, positioning glutathione insufficiency as a primary upstream disturbance rather than a downstream consequence of disease (1-3)

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In APP/PS1 (Amyloid Precursor Protein/Presenilin 1) transgenic mice, a well-characterized transgenic model of AD, HTyr treatment improves performance in the Morris water maze test, reduces cortical and hippocampal apoptosis, and restores synaptic integrity (42)

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