However, the integration between inflammation and AD is not so simple, as it has been demonstrated that stimulation of pro-inflammatory TLR4 with monophosphoryl lipid A (MLA) results in Aβ phagocytosis by microglia in vitro, as well as a decrease in Aβ load and cognitive impairment in the APP/PS1 mouse model [105]. The gene discussed is TLR4; the disease is Alzheimer disease.