Moreover, MyD88 deficiency enhances Aβ phagocytosis by microglia/macrophages in vitro and bone marrow reconstitution by MyD88-deficient cells reduces Aβ load and improves cognitive functions more efficiently compared with MyD88-sufficient cells in AD mouse models including APP/PS1 and TgCRND8 mice (100). This evidence concerns the gene MYD88 and Alzheimer disease.