Moreover, a study investigating the transcriptomic changes in AD-associated astrocytes and microglia in the brains of mice fed HFDs and humans with AD revealed that three shared genes were upregulated in both HFDs and AD including C4b, Kcnj2, and Ddr1, which mediate synaptic pruning, microglia proliferation, migration, and the inflammatory response, suggesting a mechanism through which HFDs cause AD [222]. The gene discussed is DDR1; the disease is Alzheimer disease.