CD36 and Alzheimer disease: Microglia from aged PS1-APP mice have a 2–5 fold decrease in the expression of the Aβ-binding scavenger receptors RAGE, scavenger receptor A and CD36 compared to their littermate controls (Hickman et al., 2008), which indicates microglial dysfunction in AD and supports the idea that microglia senescence contributes to the pathogenesis of AD.