The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Neuroinflammation‐induced acceleration of amyloid deposition in the APPV717F transgenic mouse
Abstract
It has been postulated that neuroinflammation plays a critical role in the pathogenesis of Alzheimer's disease (AD). To directly test whether an inflammatory stimulus can accelerate amyloid deposition in vivo, we chronically administered the bacterial endotoxin, lipopolysaccharide (LPS), intracerebroventricularly (i.c.v.) to 2‐month‐old APP V717F+/+ transgenic (TG) mice, which overexpress a mutant human amyloid precursor protein (APP 717V‐F) with or without apolipoprotein E (apoE) for 2 weeks. Two weeks following central LPS administration a striking global reactive astrocytosis with increased GFAP immunoreactivity was found throughout the brains of all LPS‐treated wild‐type and transgenic mice including the contralateral brain hemisphere. Localized microglial activation was also evident from lectin immunostaining adjacent to the cannula track of LPS‐treated mice. Quantification of thioflavine‐S‐positive Aβ deposits revealed a marked acceleration of amyloid deposition in LPS‐treated APP V717F+/+–apoE+/+ mice compared to nontreated or vehicle‐treated APP V717F+/+–apoE+/+ mice (P = 0.005). By contrast, no amyloid deposits were detected by thioflavine‐S staining in LPS or vehicle‐treated apoE‐deficient APP V717F TG mice. Our data suggest that neuroinflammation can accelerate amyloid deposition in the APP V717F+/+ mouse model of AD and that this process requires the expression of apoE.
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“However, other studies have suggested that inhibition of inflammation attenuates amyloid-β pathology35–37.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [37]
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- 10.1002/1531-8249(200003)47:3<365::AID-ANA13>3.0.CO;2-G · DOI
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Exposition aux endotoxines : influence de l'alimentation et rôle dans le vieillissement cognitif
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Metadata
- Authors
- Qiao, X., Cummins, D. J., & Paul, S. M.
- Affiliations
- Louisiana State University (US)
- Eli Lilly (United States) (US)
- Corresponding author
- Paul, Steven M.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2001-08
- Volume
- 14
- Issue
- 3
- Pages
- 474-482
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2048400917
- Cited by
- 119
- References
- 43
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 3 · 2020: 7 · 2019: 3 · 2018: 5 · 2017: 1 · 2016: 4 · 2015: 4 · 2014: 5 · 2013: 3 · 2012: 11
- FWCI
- 4.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- 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
- neuroinflammation, amyloid deposition, Alzheimer's disease, lipopolysaccharide, reactive astrogliosis, microglial activation, apolipoprotein E, amyloid precursor protein, intracerebroventricular administration
- MeSH terms
- Amyloid, Animals, Apolipoproteins E, Encephalitis, Fluorescent Dyes, Immunohistochemistry, Injections, Intraventricular, Lipopolysaccharides, Male, Mice, Transgenic, Neuroglia, RNA, Messenger, Thiazoles, Amyloid beta-Protein Precursor, Mice, Benzothiazoles
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