This repolarization of the microglial inflammatory profile to a homeostatic phenotype has been also observed after the inhibition of CSF1R in the APP/PS1 model of AD (Olmos-Alonso et al., 2016) and other models of neurodegenerative diseases such as multiple sclerosis (Nissen et al., 2018) and a model of Parkinson’s disease (PD; Neal et al., 2020). This evidence concerns the gene CSF1R and Alzheimer disease.