Cited by 389Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsAnesthesia and Neurotoxicity Research

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Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid β peptide in APPswe transgenic mice

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Sheng, J·2003·Neurobiology of Disease

DOI 10.1016/s0969-9961(03)00069-x

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Abstract

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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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)
DOI: 10.1016/s0969-9961(03)00069-x
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: cc-by-sa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid β peptide in APPswe transgenic mice

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