ArticleJournal of Alzheimer's disease : JAD2015
Restoration of lipoxin A4 signaling reduces Alzheimer's disease-like pathology in the 3xTg-AD mouse model.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The trial behind it
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Who cites it
48 citing papers in PubMed, 92 citations in OpenAlex.
- A randomized placebo-controlled trial of nicotinamide riboside in older adults with mild cognitive impairment.GeroScience · 2024Trial
- Nutritional Mushroom Treatment in Meniere's Disease withInternational journal of molecular sciences · 2019Trial
- Effects of n-3 FA supplementation on the release of proresolving lipid mediators by blood mononuclear cells: the OmegAD study.Journal of lipid research · 2015Trial
- Bioactive Anti-Inflammatory Compounds and Therapeutic Strategies for Promoting Resolution.Pharmaceutics · 2026Review
- Lipoxins as Modulators of Diseases.Cells · 2025Review
- Nanostructured Lipoxin A4: Understanding Its Biological Behavior and Impact on Alzheimer's Disease (Proof of Concept).Pharmaceutics · 2025Article
- Lipid metabolism, remodelling and intercellular transfer in the CNS.Nature reviews. Neuroscience · 2025Review
- Highlighting the Effect of Pro-inflammatory Mediators in the Pathogenesis of Periodontal Diseases and Alzheimer's Disease.Journal of pharmacy & bioallied sciences · 2024Review
- Lipoxins AJournal of neuroinflammation · 2024Article
- New insights in lipid metabolism: potential therapeutic targets for the treatment of Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Cerebrospinal Fluid Profile of Lipid Mediators in Alzheimer's Disease.Cellular and molecular neurobiology · 2023Article
- Lipid metabolism and Alzheimer's disease: clinical evidence, mechanistic link and therapeutic promise.The FEBS journal · 2023Review
- Article
- Age-linked suppression of lipoxin A4 associates with cognitive deficits in mice and humans.Translational psychiatry · 2022Article
- Specialized Pro-Resolving Mediators in Neuroinflammation: Overview of Studies and Perspectives of Clinical Applications.Molecules (Basel, Switzerland) · 2022Review
- Lipidomics of Bioactive Lipids in Alzheimer's and Parkinson's Diseases: Where Are We?International journal of molecular sciences · 2022Review
- Susceptibility of Female Mice to the Dietary Omega-3/Omega-6 Fatty-Acid Ratio: Effects on Adult Hippocampal Neurogenesis and Glia.International journal of molecular sciences · 2022Article
- Intranasal delivery of pro-resolving lipid mediators rescues memory and gamma oscillation impairment in AppCommunications biology · 2022Article
- Dementia and the Risk of Periodontitis: A Population-Based Cohort Study.Journal of dental research · 2022Article
- Lipoxins in the Nervous System: Brighter Prospects for Neuroprotection.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The initiation of an inflammatory response is critical to the survival of an organism. However, when inflammation fails to reach resolution, a chronic inflammatory state may occur, potentially leading to bystander tissue damage. Accumulating evidence suggests that chronic inflammation contributes to the progression of Alzheimer's disease (AD), and identifying mechanisms to resolve the pro-inflammatory environment stimulated by AD pathology remains an area of active investigation. Previously, we found that treatment with the pro-resolving mediator aspirin-triggered lipoxin A4 (ATL), improved cognition, reduced Aβ levels, and enhanced microglia phagocytic activity in Tg2576 transgenic AD mice. Here, we evaluated the effect of aging on brain lipoxin A4 (LXA4) levels using non-transgenic and 3xTg-AD mice. Additionally, we investigated the effect of ATL treatment on tau pathology in 3xTg-AD mice. We found that LXA4 levels are reduced with age, a pattern significantly more impacted in 3xTg-AD mice. Moreover, ATL delivery enhanced the cognitive performance of 3xTg-AD mice and reduced Aβ levels, as well as decreased the levels of phosphorylated-tau (p-tau). The decrease in p-tau was due in part to an inhibition of the tau kinases GSK-3β and p38 MAPK. In addition, microglial and astrocyte reactivity was inhibited by ATL treatment. Our results suggest that the inability to resolve the immune response during aging might be an important feature that contributes to AD pathology and cognitive deficits. Furthermore, we demonstrate that activation of LXA4 signaling could serve as a potential therapeutic target for AD-related inflammation and cognitive dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.