TLR4 and Alzheimer disease: The Mo/Hu APPswe PS1dE9 mice, which are homozygous for a destructive mutation of TLR4 (TlrLps-d/TlrLps-d), showed increased diffuse and fibrillar Aβ deposits compared to TLR4-WT mouse models [41], indicating that manipulation of the innate immune responses via the TLR4 axis may decrease Aβ load and cell injuries in AD brain.