ArticleNature communications2020
N-AS-triggered SPMs are direct regulators of microglia in a model of Alzheimer's disease.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
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- Methylomic signatures of tau and amyloid-beta in transgenic mouse models of Alzheimer's disease neuropathology.NPJ dementia · 2026Article
- Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions.Molecular neurodegeneration · 2025Review
- Specialized pro-resolving mediators in vascular inflammation and atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Astrocyte-derived clusterin disrupts glial physiology to obstruct remyelination in mouse models of demyelinating diseases.Nature communications · 2024Article
- Notoginsenoside R1 ameliorates the inflammation induced by amyloid‑β by suppressing SphK1‑mediated NF‑κB activation in PC12 cells.Molecular medicine reports · 2024Article
- Microglia as a Possible Alternative Therapeutic for Dementia.Journal of Alzheimer's disease reports · 2024Review
- Inhibition of microfold cells ameliorates early pathological phenotypes by modulating microglial functions in Alzheimer's disease mouse model.Journal of neuroinflammation · 2023Article
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
- Possibility of averting cytokine storm in SARS-COV 2 patients using specialized pro-resolving lipid mediators.Biochemical pharmacology · 2023Review
- Cerebrospinal Fluid Profile of Lipid Mediators in Alzheimer's Disease.Cellular and molecular neurobiology · 2023Article
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
- Trilobatin rescues cognitive impairment of Alzheimer's disease by targeting HMGB1 through mediating SIRT3/SOD2 signaling pathway.Acta pharmacologica Sinica · 2022Article
- Metabolic and Cellular Compartments of Acetyl-CoA in the Healthy and Diseased Brain.International journal of molecular sciences · 2022Review
- Astrocytic and microglial cells as the modulators of neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2022Review
- MiR-214-3p Prevents the Development of Perioperative Neurocognitive Disorders in Elderly Rats.Current medical science · 2022Article
- Specialized Pro-Resolving Mediators in Neuroinflammation: Overview of Studies and Perspectives of Clinical Applications.Molecules (Basel, Switzerland) · 2022Review
- Intranasal delivery of pro-resolving lipid mediators rescues memory and gamma oscillation impairment in AppCommunications biology · 2022Article
- Discovery of a dual-action small molecule that improves neuropathological features of Alzheimer's disease mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- E-series resolvin metabolome, biosynthesis and critical role of stereochemistry of specialized pro-resolving mediators (SPMs) in inflammation-resolution: Preparing SPMs for long COVID-19, human clinical trials, and targeted precision nutrition.Seminars in immunology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingosine kinase1 (SphK1) is an acetyl-CoA dependent acetyltransferase which acts on cyclooxygenase2 (COX2) in neurons in a model of Alzheimer's disease (AD). However, the mechanism underlying this activity was unexplored. Here we show that N-acetyl sphingosine (N-AS) is first generated by acetyl-CoA and sphingosine through SphK1. N-AS then acetylates serine 565 (S565) of COX2, and the N-AS-acetylated COX2 induces the production of specialized pro-resolving mediators (SPMs). In a mouse model of AD, microglia show a reduction in N-AS generation, leading to decreased acetyl-S565 COX2 and SPM production. Treatment with N-AS increases acetylated COX2 and N-AS-triggered SPMs in microglia of AD mice, leading to resolution of neuroinflammation, an increase in microglial phagocytosis, and improved memory. Taken together, these results identify a role of N-AS in the dysfunction of microglia in AD.
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