Sustained Alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe/PS1 mice.

BACKGROUND Most Alzheimer's disease (AD) cases arise sporadically and may involve innate immune activation of microglial expressed Toll-like receptors regulated through the myeloid differentiation protein 88 (MyD88) pathway. OBJECTIVE It was the aim of this study to test the innate immune involvement in AD pathology. METHODS We mated APPsw/PS1ΔE9 mice with MyD88-deficient mice. RESULTS Progeny mice had similar levels of soluble amyloid-β peptides, amyloid plaque density and neuroimmune staining patterns. However, double-transgenic mice did show a significantly reduced life expectancy. CONCLUSION Our findings indicate that impaired innate immune responses may play a role in AD pathology.