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TB-500’s key mechanisms include: Actin sequestration: By binding G-actin (monomeric actin), TB-500 keeps it available for cell migration and wound repair rather than polymerizing prematurely into structural filaments

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These results underscore a reduction in Tau phosphorylation within the brain, particularly in CA1 neurons, highlighting the potential of selenate as a therapeutic agent in modulating Tau pathology in Alzheimer's disease