For instance, CCL2‐CCR2 signaling between microglia and astrocytes is implicated in neuroinflammation, with its upregulation causing cognitive dysfunction.[38] Moreover, astrocyte‐derived IL‐3 reprograms microglia to increase IL‐3Rα expression, boosting the capacity of microglia to clear Aβ and tau protein aggregates, thereby improving AD pathology.[39] Meanwhile, complement‐dependent intercellular crosstalk has also been identified, where astrocytic NF‐κB signaling elicits the extracellular release of C3. This evidence concerns the gene NFKB1 and Alzheimer disease.