ArticleCell communication and signaling : CCS2024
N-acetylaspartate mitigates pro-inflammatory responses in microglial cells by intersecting lipid metabolism and acetylation processes.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- From neuronal marker to metabolic mediator: Expanding the functional landscape of N-acetylaspartate in the central nervous system and the periphery.Neural regeneration research · 2026Article
- Bifidobacterium animalis subsp. lactis and Enterococcus hirae Enhance Immunity by Modulating Gut Microbiota and Metabolic Pathways in Immunosuppressed Mice.Probiotics and antimicrobial proteins · 2026Article
- The regulatory role of post-translational modifications in the pathogenesis of ulcerative colitis.Molecular biology reports · 2026Review
- The Emerging Role of N-Acetylaspartate in Cancer.International journal of molecular sciences · 2026Review
- Review
- Immunometabolic Regulation of Neuroinflammation in Retinitis Pigmentosa: Roles of Microglia, Müller Glia, and Regulated Cell Death.Biomolecules · 2026Review
- Post-translational modifications regulating microglial inflammation in central nervous system disorders: a review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Higher Serum Aspartate May be Associated with Better Cognitive Function as Mediated by Reduced Aβ Accumulation in Frontal and Temporal Lobes in Mild Cognitive Impairment.Journal of molecular neuroscience : MN · 2025Article
- MicroRNA- 3135b as a Therapeutic Target and Clinical Biomarker for Stroke: Regulation of the NF-κB/IKKβ Signaling Pathway.Molecular neurobiology · 2025Article
- Oxidative Stress in Neurodegenerative Disorders: A Key Driver in Impairing Skeletal Muscle Health.International journal of molecular sciences · 2025Review
- Aspartate in the Brain: A Review.Neurochemical research · 2025Review
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9 authors.
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Abstract
backgroundMicroglia play a crucial role in brain development and repair by facilitating processes such as synaptic pruning and debris clearance. They can be activated in response to various stimuli, leading to either pro-inflammatory or anti-inflammatory responses associated with specific metabolic alterations. The imbalances between microglia activation states contribute to chronic neuroinflammation, a hallmark of neurodegenerative diseases. N-acetylaspartate (NAA) is a brain metabolite predominantly produced by neurons and is crucial for central nervous system health. Alterations in NAA metabolism are observed in disorders such as Multiple Sclerosis and Canavan disease. While NAA's role in oligodendrocytes and astrocytes has been investigated, its impact on microglial function remains less understood.
methodsThe murine BV2 microglial cell line and primary microglia were used as experimental models. Cells were treated with exogenous NAA and stimulated with LPS/IFN-γ to reproduce the pro-inflammatory phenomenon. HPLC and immunofluorescence analysis were used to study lipid metabolism following NAA treatment. Automated fluorescence microscopy was used to analyze phagocytic activity. The effects on the pro-inflammatory response were evaluated by analysis of protein/mRNA expression and ChIP assay of typical inflammatory markers.
resultsNAA treatment promotes an increase in both lipid synthesis and degradation, and enhances the phagocytic activity of BV2 cells, thus fostering surveillant microglia characteristics. Importantly, NAA decreases the pro-inflammatory state induced by LPS/IFN-γ via the activation of histone deacetylases (HDACs). These findings were validated in primary microglial cells, highlighting the impact on cellular metabolism and inflammatory responses.
conclusionsThe study highlighted the role of NAA in reinforcing the oxidative metabolism of surveillant microglial cells and, most importantly, in buffering the inflammatory processes characterizing reactive microglia. These results suggest that the decreased levels of NAA observed in neurodegenerative disorders can contribute to chronic neuroinflammation.
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