β-Amyloid peptide potentiates inflammatory responses induced by lipopolysaccharide, interferon -γ and 'advanced glycation endproducts' in a murine microglia cell line

Summary β‐Amyloid (Aβ) plaques are characteristic hallmarks of Alzheimer's disease (AD). In AD, it has been suggested that activation of microglial cells might be the link between Aβ deposition and neuronal degeneration. Activated microglia are associated with senile plaques and produce free ra...

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Veröffentlicht in:	The European journal of neuroscience 2003-02, Vol.17 (4), p.813-821
Hauptverfasser:	Gasic-Milenkovic, Jovana, Dukic-Stefanovic, Sladjana, Deuther-Conrad, Winnie, Gaertner, Ullrich, Muench, Gerald
Format:	Artikel
Sprache:	eng
Schlagworte:	ageing Alzheimer's disease Amyloid - ultrastructure Amyloid beta-Peptides - chemistry Amyloid beta-Peptides - pharmacology Animals Cell Line Cell Survival Dose-Response Relationship, Drug Drug Synergism Glycation End Products, Advanced - pharmacology Inflammation - etiology Inflammation - metabolism Inflammation - physiopathology Interferon-gamma - pharmacology interleukin-6 Interleukin-6 - metabolism Lipopolysaccharides - pharmacology Macrophage Colony-Stimulating Factor - metabolism macrophage-colony stimulating factor Mice Microglia - cytology Microglia - drug effects Microscopy, Electron - methods Nitric Oxide - metabolism oxidative stress Peptide Biosynthesis Peptide Fragments - chemistry Peptide Fragments - pharmacology Plaque, Amyloid - ultrastructure Tumor Necrosis Factor-alpha - metabolism
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