The reported similar activity of the CSF1R pathway in experimental models of AD and prion disease, human prion disease (variant Creutzfeldt-Jakob disease; vCJD) and human AD, suggests common pathways controlling microglial proliferation and activation in chronic neurodegeneration (Gomez-Nicola and others 2013) (Fig. 2). The gene discussed is CSF1R; the disease is prion disease.