Fuhrmann et al. [92] crossed AD mice with transgenic mice (3XTg, CX3CR1-GFP, and Thy1-YFP) lacking the CX3CR1 receptor (3XTg:CX3CR1−/−:Thy1-YFP) and showed significant synapse loss in addition to attenuated microglial migratory velocity, indicating a critical role for the CX3CR1 chemokine receptor in microglia-mediated neuronal circuits in AD. Here, THY1 is linked to Alzheimer disease.