We previously demonstrated that an AD mouse model (Mo/Hu APPswe PS1dE9 mice) homozygous for a destructive mutation of TLR4 (TlrLps-d/TlrLps-d) had increases in diffuse and fibrillar Aβ deposits as well as buffer-soluble and insoluble Aβ in the brain as compared with a TLR4 wild-type AD model mice [17]. The gene discussed is TLR4; the disease is Alzheimer disease.