Our current hypothesis is that within the context of AD, PLX5622 treatment not only eliminates Csf1r-expressing microglial cells responsible for most of Cxcl16 production, but at the same time induces expression of Cxcl16 in other brain-resident (e.g. PLX5622-resistant microglia) or newly recruited myeloid cells, or even non-myeloid cells of the CNS. This evidence concerns the gene CXCL16 and Alzheimer disease.