In the healthy brain, APOE is mainly produced by astrocytes, but in Alzheimer's disease (AD), reactive microglia greatly increase APOE expression. APOE from microglia binds to TREM2 on their surface in pathological conditions, regulating their response to Aβ and tau pathology. This interaction influences microglial migration to Aβ plaques, phagocytosis, and inflammation, affecting AD progression. To support AD drug development, we provide key target proteins like APOE, TREM2, Aβ, and Tau, essential for advancing therapeutic strategies for AD. |