The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease
Open accessAbstract
The major histopathological hallmarks of Alzheimer’s disease (AD) include β-amyloid (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Aβ 1–42 (Aβ 1-42) has been shown to induce neurotoxicity and secretion of proinflammatory mediators that potentiate neurotoxicity. Proinflammatory and neurotoxic activities of Aβ 1-42 were shown to be mediated by interactions with several cell surface receptors, including the chemotactic G protein-coupled N-formyl peptide receptor 2 (FPR2). The present study investigated the impact of a new FPR2 agonist, MR-39, on the neuroinflammatory response in ex vivo and in vivo models of AD. To address this question, organotypic hippocampal cultures from wild-type (WT) and FPR2-deficient mice (knockout, KO, FPR2−/−) were treated with fibrillary Aβ 1-42, and the effect of the new FPR2 agonist MR-39 on the release of pro- and anti-inflammatory cytokines was assessed. Similarly, APP/PS1 double-transgenic AD mice were treated for 20 weeks with MR-39, and immunohistological staining was performed to assess neuronal loss, gliosis, and Aβ load in the hippocampus and cortex. The data indicated that MR-39 was able to reduce the Aβ 1-42-induced release of proinflammatory cytokines and to improve the release of anti-inflammatory cytokines in mouse hippocampal organotypic cultures. The observed effect was apparently related to the inhibition of the MyD88/TRAF6/NFкB signaling pathway and a decrease in NLRP3 inflammasome activation. Administration of MR-39 to APP/PS1 mice improved neuronal survival and decreased microglial cell density and plaque load. These results suggest that FPR2 may be a promising target for alleviating the inflammatory process associated with AD and that MR-39 may be a useful therapeutic agent for AD.
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Deficiency of FPR2 or administration of its inhibitors/anti-inflammatory ligands alleviates pathological symptoms of AD, including reduced activation of glial cells and tau hyperphosphorylation, and ultimately improves cognitive function.
“Deficiency of FPR2 or administration of its inhibitors/anti-inflammatory ligands could alleviate the pathological symptoms of AD, including reduced activation of glial cells (microglia and/or astrocytes) and tau hyperphosphorylation, and ultimately leading to improvement in cognitive function [151–154].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [154]
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Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation
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- Authors
- Trojan, E., Tylek, K., Schröder, N., Kahl, I., Brandenburg, L.-O., Mastromarino, M., Leopoldo, M., Basta-Kaim, A., & Lacivita, E.
- Affiliations
- Maj Institute of Pharmacology (PL)
- Universitätsmedizin Rostock (DE)
- University of Bari Aldo Moro (IT)
- ORCID
- Venue
- Molecular Neurobiology
- Published
- 2021-09-01
- Volume
- 58
- Issue
- 12
- Pages
- 6203-6221
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- PMC
- PMC8639560
- OpenAlex
- W3198178969
- Cited by
- 26
- References
- 74
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 5 · 2023: 4 · 2022: 5
- FWCI
- 2.36
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Molecular Neurobiology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion, other-oa)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, other-oa)
- Funders
- Alzheimer's Association (AARG-NTF-18-565227)
- Narodowe Centrum Nauki (2017/26/M/NZ7/01048 (HARMONIA))
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, amyloid-beta 42, neuroinflammation, inflammatory cytokines, anti-inflammatory cytokines, NLRP3 inflammasome, APP/PS1 mice, organotypic hippocampal slice cultures, microglia, gliosis, neuroprotection
- MeSH terms
- Neuroinflammatory Diseases, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Disease Models, Animal, Hippocampus, Male, Mice, Transgenic, Peptide Fragments, Amyloid beta-Peptides, Receptors, Formyl Peptide, Mice
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