Source:http://linkedlifedata.com/resource/pubmed/id/13678674
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2003-9-18
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pubmed:abstractText |
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 beta peptide (Abeta). APPswe transgenic (Tg) mice were treated with either LPS or phosphate-buffered saline (PBS). In LPS-treated APPswe mice, Abeta1-40/42 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 Abeta- and APP-immunoreactive neurons (Abeta(+) and APP(+) neurons) increased significantly in LPS-treated APPswe mice; APP(+) and Abeta(+) 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 Abeta. It remains to be seen whether such events can cause neuronal dysfunction/degeneration and, with time, lead to extracellular Abeta deposits, as they occur in Alzheimer's disease.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Protein Precursor,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-40),
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-42)
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0969-9961
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
133-45
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:13678674-Alzheimer Disease,
pubmed-meshheading:13678674-Amyloid beta-Peptides,
pubmed-meshheading:13678674-Amyloid beta-Protein Precursor,
pubmed-meshheading:13678674-Animals,
pubmed-meshheading:13678674-Encephalitis,
pubmed-meshheading:13678674-Intracellular Fluid,
pubmed-meshheading:13678674-Lipopolysaccharides,
pubmed-meshheading:13678674-Mice,
pubmed-meshheading:13678674-Mice, Inbred C3H,
pubmed-meshheading:13678674-Mice, Inbred C57BL,
pubmed-meshheading:13678674-Mice, Transgenic,
pubmed-meshheading:13678674-Peptide Fragments
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pubmed:year |
2003
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pubmed:articleTitle |
Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid beta peptide in APPswe transgenic mice.
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pubmed:affiliation |
Department of Pathology (Division of Neuropathology), The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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