Anti-inflammatory/anti-amyloidogenic effects of plasmalogens in lipopolysaccharide-induced neuroinflammation in adult mice
Open accessAbstract
BACKGROUND: Neuroinflammation involves the activation of glial cells in neurodegenerative diseases such as Alzheimer's disease (AD). Plasmalogens (Pls) are glycerophospholipids constituting cellular membranes and play significant roles in membrane fluidity and cellular processes such as vesicular fusion and signal transduction. METHODS: In this study the preventive effects of Pls on systemic lipopolysaccharide (LPS)-induced neuroinflammation were investigated using immunohistochemistry, real-time PCR methods and analysis of brain glycerophospholipid levels in adult mice. RESULTS: Intraperitoneal (i.p.) injections of LPS (250 μg/kg) for seven days resulted in increases in the number of Iba-1-positive microglia and glial fibrillary acidic protein (GFAP)-positive astrocytes in the prefrontal cortex (PFC) and hippocampus accompanied by the enhanced expression of IL-1β and TNF-α mRNAs. In addition, β-amyloid (Aβ3-16)-positive neurons appeared in the PFC and hippocampus of LPS-injected animals. The co-administration of Pls (i.p., 20 mg/kg) after daily LPS injections significantly attenuated both the activation of glial cells and the accumulation of Aβ proteins. Finally, the amount of Pls in the PFC and hippocampus decreased following the LPS injections and this reduction was suppressed by co-treatment with Pls. CONCLUSIONS: These findings suggest that Pls have anti-neuroinflammatory and anti-amyloidogenic effects, thereby indicating the preventive or therapeutic application of Pls against AD.
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Chronic neuroinflammation has been shown to increase α-synuclein deposition in various synucleinopathy animal models.
“Not only has chronic neuroinflammation been shown to increase α-synuclein deposition in various synucleinopathy animal models (51–56), but when these animals were treated with drugs to reduce neuroinflammation, α-synuclein neuropathology also decreased (57, 58).”
From LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies (2020) · cites this paper as [54]
The Background and Discussion section ‘Mechanisms of LPS-induced accumulation of Aβ’ describe neuroinflammation and β-amyloid accumulation in mice, not α-synuclein deposition. Searches for α-synuclein and synucleinopathy found no passage addressing deposition in synucleinopathy animal models. The cited paper’s copy therefore does not verify this claim. (LLM, conf=0.73)
Experimental — accuracy not yet measuredPlasmalogens suppress microglia activation after systemic LPS injection in mice.
“This concept is also supported by the finding that plasmalogens suppress microglia activation after systemic injection of lipopolysaccharides (LPS) in mice [221,222].”
From Peroxisomes in brain development and function (2016) · cites this paper as [221]
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- Authors
- Ifuku, M., Katafuchi, T., Mawatari, S., Noda, M., Miake, K., Sugiyama, M., & Fujino, T.
- Affiliations
- Kyushu University (JP)
- Institute of Rheological Functions of Food (JP)
- Marudai FOOD Co., Ltd. (Japan) (JP)
- Corresponding author
- Katafuchi, Toshihiko
- Venue
- Journal of Neuroinflammation
- Published
- 2012-08-13
- Volume
- 9
- Issue
- 1
- Pages
- 197-197
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3444880
- OpenAlex
- W2037650763
- Cited by
- 130
- References
- 60
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 13 · 2023: 8 · 2022: 12 · 2021: 15 · 2020: 11 · 2019: 13 · 2018: 12 · 2017: 9 · 2016: 6 · 2015: 6 · 2014: 5 · 2013: 5
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Japan Society for the Promotion of Science (22590084, 22590225)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- plasmalogens, neuroinflammation, lipopolysaccharide, Alzheimer's disease, amyloid-beta, microglial activation, astrocytes, glycerophospholipids, prefrontal cortex, hippocampus, IL-1β, TNF-α, anti-inflammatory activity
- MeSH terms
- Animals, Anti-Inflammatory Agents, Brain Edema, Chickens, Inflammation, Lipopolysaccharides, Male, Mice, Inbred C57BL, Plasmalogens, Amyloid beta-Peptides, Glycerophospholipids, Mice
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