Sustained Alzheimer's Amyloid Pathology in Myeloid Differentiation Protein-88-Deficient APPswe/PS1 Mice

被引:6
作者
Goll, Y.
Bekenstein, U.
Barbash, S.
Greenberg, D. S.
Zangen, R.
Shoham, S.
Soreq, H. [1 ]
机构
[1] Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel
关键词
Alzheimer's disease; Amyloid-beta; APPsw/PS1 Delta E9 mice; Toll-like receptor; Myeloid differentiation protein 88; DISEASE; PROTEIN; DEGRADATION; MICROGLIA; PLAQUES; DEATH; MODEL;
D O I
10.1159/000353689
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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/PS1 Delta E9 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. (C) 2013 S. Karger AG, Basel
引用
收藏
页码:58 / 60
页数:3
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