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Sustained Alzheimer's Amyloid Pathology in Myeloid Differentiation Protein-88-Deficient APPswe/PS1 Mice
被引:6
作者:

Goll, Y.
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机构: Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel

Bekenstein, U.
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机构: Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel

Barbash, S.
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h-index: 0
机构: Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel

Greenberg, D. S.
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h-index: 0
机构: Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel

Zangen, R.
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机构: Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel

Shoham, S.
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机构: Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel

Soreq, H.
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机构:
Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel Hebrew Univ Jerusalem, Dept Biol Chem, IL-91904 Jerusalem, Israel
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
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页码:58 / 60
页数:3
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