TLR4 and Alzheimer disease: We previously demonstrated that an AD mouse model homozygous for a nonfunctional (loss-of-function) mutation of TLR4 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 mouse model (TgAPPswe/PS1dE9 mice) at 14-16 months of age [10].