RvE1 treatment prevents memory loss and neuroinflammation in the Ts65Dn mouse model of Down syndrome
Open accessAbstract
Inflammation can be resolved by pro‐homeostatic lipids called specialized pro‐resolving mediators (SPMs) upon activation of their receptors. Dysfunctional inflammatory resolution is now considered as a driver of chronic neuroinflammation and Alzheimer's disease (AD) pathogenesis. We have previously shown that SPM levels were reduced and also that SPM‐binding receptors were increased in patients with AD compared to age‐matched controls. Individuals with Down syndrome (DS) exhibit accelerated acquisition of AD neuropathology, dementia, and neuroinflammation at an earlier age than the general population. Beneficial effects of inducing resolution in DS have not been investigated previously. The effects of the SPM resolvin E1 (RvE1) in a DS mouse model (Ts65Dn) were investigated with regard to inflammation, neurodegeneration, and memory deficits. A moderate dose of RvE1 for 4 weeks in middle‐aged Ts65Dn mice elicited a significant reduction in memory loss, along with reduced levels of serum pro‐inflammatory cytokines, and reduced microglial activation in the hippocampus of Ts65Dn mice but had no effects in age‐matched normosomic mice. There were no observable adverse side effects in Ts65Dn or in normosomic mice. These findings suggest that SPMs may represent a novel drug target for individuals with DS and others at risk of developing AD.
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Pro-resolving ligands or inhibitors of CMKLR1 attenuate inflammatory responses, including neuroinflammation.
“Pro-resolving ligands or inhibitors of CMKLR1 have been shown to attenuate inflammatory responses, including neuroinflammation [156–158].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [156]
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References 55 · Cited by 34
Research works printed but not linked: 1
- PubChem. National Center for Biotechnology Information. Compound Database. CID=10473088. https://pubchem.ncbi.nlm.nih.gov/compound/10473088, 2018.
- Authors
- Hamlett, E. D., Hjorth, E., Ledreux, A., Gilmore, A., Schultzberg, M., & Granholm, A. C.
- Affiliations
- Medical University of South Carolina (US)
- Karolinska Institutet (SE)
- University of Denver (US)
- Corresponding author
- Hamlett, Eric D.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2020-01-16
- Volume
- 68
- Issue
- 7
- Pages
- 1347-1360
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC7205572
- OpenAlex
- W3000096681
- Cited by
- 34
- References
- 55
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 1 · 2023: 5 · 2022: 8 · 2021: 3 · 2020: 9
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Alzheimer's Association (DSADIIP‐13‐284845)
- Fondation Jérôme Lejeune
- National Institute on Aging (R21AG048631)
- Hjärnfonden
- Vetenskapsrådet (22743, 22744)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- resolvin E1, specialized pro-resolving mediators, Down syndrome, Ts65Dn mouse model, neuroinflammation, memory loss, Alzheimer's disease, microglial activation, hippocampus, inflammatory cytokines, neurodegeneration, inflammation resolution
- MeSH terms
- Alzheimer Disease, Animals, Down Syndrome, Hippocampus, Male, Memory Disorders, Mice, Transgenic, Eicosapentaenoic Acid, Maze Learning
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