Neuroinflammation‐induced acceleration of amyloid deposition in the APPV717F transgenic mouse

Qiao, Xiaoxi; Cummins, David J.; Paul, Steven M.

doi:10.1046/j.0953-816x.2001.01666.x

Cited by 119Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

Neuroinflammation‐induced acceleration of amyloid deposition in the APPV717F transgenic mouse

Qiao, Xiaoxi, Cummins, David J., Paul, Steven M.·2001·European Journal of Neuroscience

DOI 10.1046/j.0953-816x.2001.01666.x

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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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Authors: Qiao, X., Cummins, D. J., & Paul, S. M.
Affiliations: Louisiana State University (US)
Eli Lilly (United States) (US)
Corresponding author: Paul, Steven M.
ORCID: Qiao, Xiaoxi
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
DOI: 10.1046/j.0953-816x.2001.01666.x
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 141 d)
Locations: European Journal of Neuroscience (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › 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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Neuroinflammation‐induced acceleration of amyloid deposition in the APPV717F transgenic mouse

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