In a model of tauopathy, widespread ablation of myeloid cells that depend on CSF1R signalling (including microglia, BAMs, and dendritic cells) was shown to almost completely prevent tau-mediated neurodegeneration in mice expressing APOE4 [172], suggesting that CNS innate immunity might be playing opposite roles when it comes to controlling Aβ pathology or tau-driven neurodegeneration. Here, CSF1R is linked to tauopathy.