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/PS1DeltaE9 mice with MyD88-deficient mice. RESULTS: Progeny mice had similar levels of soluble amyloid-beta 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.
        
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Goll Y, Bekenstein U, Barbash S, Greenberg DS, Zangen R, Shoham S, Soreq H (2014) Sustained Alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe/PS1 mice Neurodegener Dis13: 58-60
Goll Y, Bekenstein U, Barbash S, Greenberg DS, Zangen R, Shoham S, Soreq H (2014) Neurodegener Dis13: 58-60