The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid β peptide in APPswe transgenic mice
Open accessAbstract
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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“However, nonspecific microglia activation induced by lipopolysaccharide does not have the same amyloid-promoting effect as myelin dysfunction, as increases, decreases or no changes in amyloid burden have been reported48–51.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [50]
In the citing paper
“lipopolysaccharide (a major gram negative bacterial cell wall component)-induced inflammation in mice with amyloidosis or tauopathy increased neuropathology [187, 283]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [283]
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Metadata
- Authors
- Sheng, J.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Sheng, J
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2003-10
- Volume
- 14
- Issue
- 1
- Pages
- 133-145
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2023136593
- Cited by
- 388
- References
- 51
- Citations by year
- 2026: 6 · 2025: 18 · 2024: 17 · 2023: 18 · 2022: 27 · 2021: 26 · 2020: 23 · 2019: 15 · 2018: 23 · 2017: 14 · 2016: 24 · 2015: 18 · 2014: 20 · 2013: 18 · 2012: 26
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute on Aging (P50AG005146, AG 05146)
- National Institute of Neurological Disorders and Stroke (T32NS07435, T32NS007435)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
- Keywords
- lipopolysaccharide, neuroinflammation, amyloid precursor protein, amyloid-beta, microglia, F4/80, APP processing, Alzheimer's disease, neocortex
- MeSH terms
- Alzheimer Disease, Animals, Encephalitis, Intracellular Fluid, Lipopolysaccharides, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice
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