Suppressing CD200/CD200R signaling via genetic approaches (deleting Cd200) impairs long-term potentiation (LTP) [16], whereas pharmaceutical approaches (using CD200Fc, a CD200R agonist) that activate CD200/CD200R signaling significantly enhance synaptic plasticity in AD and aged mice by regulating inflammation [17–19]. This evidence concerns the gene CD200 and Alzheimer disease.