Deletion of CD14, which acts as a co-receptor for LPS along with TLR2 and TLR4, in APP/PS1 mice reduced total microglial numbers, in particular CD45-positive microglia, attenuated AD pathology whilst also increasing the expression of TNF-α and IL-10, suggesting an induction of a shift of activation of microglia towards the M2b state [76]. This evidence concerns the gene TLR4 and Alzheimer disease.