Additionally, GSK-3β activation promotes amyloid-beta plaque buildup, potentially triggering microglia-mediated neuroinflammation that drives AD progression.531–533 Activation of the Ras-MAPK pathway further enhances gene transcription related to neuronal survival, synaptic plasticity, and tau phosphorylation, which is also linked to amyloid-beta accumulation and NFT formation.534 The mechanisms outlined above provide potential therapeutic strategies for targeting insulin signaling pathways in AD treatment. The gene discussed is MAPT; the disease is Alzheimer disease.