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Intrahippocampal LPS injections reduce Aβ load in APP+PS1 transgenic mice
Abstract
Multiple lines of evidence indicate that inflammatory processes are involved in the pathogenesis of Alzheimer's disease. Lipopolysaccharide (LPS) is widely used to induce inflammation in experimental systems. Consequently we injected LPS or saline intrahippocampally in 11 and 16 months old APP+PS1 transgenic mice to induce brain inflammation, then used immunocytochemistry to examine amyloid pathology 7 days later. As expected, LPS activated microglia as indicated by a significant increase in the area covered by major histocompatibility complex-II (MHC-II) immunostaining in the mice injected with LPS compared to the saline injected. Simultaneously, Abeta immunostaining showed an unexpected reduction of the Abeta load in the mice injected with LPS compared to the saline injected. This effect of LPS on the Abeta load in APP+PS1 mice strengthens the hypothesis that moderate amounts of microglial activation may be beneficial in Alzheimer's disease, by increasing the clearance of Abeta.
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“For example, increased gliosis induced by brain infusion of lipopolysaccharide (4) or overexpression of the inflammatory cytokine interleukin-6 (5) or interferon-γ (6) markedly reduces amyloid plaque burden.”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [4]
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Metadata
- Authors
- DiCarlo, G.
- Affiliations
- University of South Florida (US)
- Corresponding author
- DiCarlo, G
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2001-12
- Volume
- 22
- Issue
- 6
- Pages
- 1007-1012
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W1993909442
- Cited by
- 223
- References
- 28
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 7 · 2023: 2 · 2022: 5 · 2021: 5 · 2020: 12 · 2019: 6 · 2018: 6 · 2017: 5 · 2016: 12 · 2015: 15 · 2014: 11 · 2013: 8 · 2012: 21
- FWCI
- 4.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG018478, AG 15490, R01AG015490, AG18478)
- 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 › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- lipopolysaccharide, Alzheimer's disease, amyloid-beta, APP/PS1 mice, microglial activation, neuroinflammation, hippocampus, MHC class II, amyloid-beta clearance, intrahippocampal injection
- MeSH terms
- Animals, Gene Expression Regulation, Genes, MHC Class II, Hippocampus, Immunohistochemistry, Lipopolysaccharides, Membrane Proteins, Mice, Transgenic, Microinjections, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Mice, Presenilin-1
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