These include the cytokine context (inflammatory milieu including IL-23 and GM-CSF in EAE, which is absent in Alzheimer’s disease-like APP/PS1 mice35), the sources and amount of IL-12 (high in MdCs in EAE and lower in glial cells in APP/PS1 mice), the nature of tissue damage (multifocal disseminated in EAE and more restricted to the cerebrum in APP/PS1 mice) as well as CNS region-specific transcriptomic changes of neuroectodermal cells. This evidence concerns the gene CSF2 and Alzheimer disease.