Sustained alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe/PS1 Mice

Y. Goll, U. Bekenstein, S. Barbash, D. S. Greenberg, R. Zangen, S. Shoham, H. Soreq

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)58-60
Number of pages3
JournalNeurodegenerative Diseases
Volume13
Issue number2-3
DOIs
StatePublished - Jan 2014

Keywords

  • Alzheimer's disease
  • Amyloid-β, APPsw/PS1ΔE9 mice
  • Myeloid differentiation protein 88
  • Toll-like receptor

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