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- W2023136593 abstract "The present study was designed to examine whether brain inflammation caused by systemic administration of lipopolysaccharides (LPS) alters the expression/processing of amyloid precursor protein (APP) and increases the generation of amyloid β peptide (Aβ). APPswe transgenic (Tg) mice were treated with either LPS or phosphate-buffered saline (PBS). In LPS-treated APPswe mice, Aβ1–40/42 was 3-fold and APP was 1.8-fold higher than those in PBS-treated mice (P < 0.05) by ELISA, Western blots and immunoprecipitation–mass spectrometry (IP–MS) ProteinChip analysis. Numbers of Aβ- and APP-immunoreactive neurons (Aβ(+) and APP(+) neurons) increased significantly in LPS-treated APPswe mice; APP(+) and Aβ(+) neurons in neocortex were associated with an increased number of F4/80-immunoreactive microglia (F4/80(+) microglia) in their anatomical environment. Our findings demonstrate that experimental neuroinflammation increases APP expression/processing and causes intracellular accumulation of Aβ. It remains to be seen whether such events can cause neuronal dysfunction/degeneration and, with time, lead to extracellular Aβ deposits, as they occur in Alzheimer’s disease." @default.
- W2023136593 created "2016-06-24" @default.
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- W2023136593 date "2003-10-01" @default.
- W2023136593 modified "2023-09-30" @default.
- W2023136593 title "Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid β peptide in APPswe transgenic mice" @default.
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- W2023136593 doi "https://doi.org/10.1016/s0969-9961(03)00069-x" @default.
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