These results provided important human evidence to understand the relationship of cytokine IL-3 with microglial activity and AD pathogenesis as well as cognitive function and supported our hypothesis that glial cell crosstalk, especially astrocyte–microglia communication, may be downstream of amyloid pathology and may play a critical role in the subsequent tau pathology and neurodegeneration as well as cognitive decline in AD (Fig. 5B). This evidence concerns the gene MAPT and amyloidosis.