CX3CR1 and Alzheimer disease: While the study by Fuhrmann and coworkers did not show differences in Aβ abundance between Cx3cr1-sufficient and -deficient mice, Lee et al. suggested that Aβ aggregates in 3x Tg-AD mice may be more intracellular than extracellular at the age at which this study was done, therefore affecting the ability of microglia to phagocytose these deposits.