As amyloid-β directly activates GSK3β, driving tau hyperphosphorylation [39,40], we assessed GSK3β-mediated tau hyperphosphorylation at serine/threonine sites via Western blot using hippocampal protein extracts from AD mice to evaluate the impact of long-term Avn-C treatment, initiated at the early AD stage, on preventing tau pathology–driven disease progression. The gene discussed is MAPT; the disease is Alzheimer disease.