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N-acetylaspartate mitigates pro-inflammatory responses in microglial cells by intersecting lipid metabolism and

Federica Felice1, Pamela De Falco1, Martina Milani1

  • 1Department of Biology, University of Rome Tor Vergata, Rome, 00133, Italy.

Cell Communication and Signaling : CCS
|November 26, 2024
PubMed
Abstract

Insights

N-acetylaspartate (NAA) enhances microglial phagocytosis and oxidative metabolism. NAA also reduces neuroinflammation by activating histone deacetylases (HDACs), suggesting its deficiency contributes to neurodegenerative diseases.

Area of Science:

  • Neuroscience
  • Immunology
  • Metabolism

Background:

  • Microglia are key immune cells in the brain, involved in development, repair, and neuroinflammation.
  • Imbalances in microglial activation states are linked to neurodegenerative diseases.
  • N-acetylaspartate (NAA) is a vital brain metabolite, but its role in microglial function is unclear.

Purpose of the Study:

  • To investigate the impact of N-acetylaspartate (NAA) on microglial function and inflammatory responses.
  • To explore NAA's potential role in modulating neuroinflammation.

Main Methods:

  • Utilized murine BV2 microglial cell line and primary microglia.
  • Administered exogenous NAA and stimulated cells with LPS/IFN-γ to induce inflammation.
  • Analyzed lipid metabolism, phagocytic activity, and pro-inflammatory marker expression.

Main Results:

  • NAA treatment increased lipid synthesis/degradation and enhanced microglial phagocytic activity.
  • NAA significantly reduced LPS/IFN-γ-induced pro-inflammatory responses via histone deacetylase (HDAC) activation.
  • Findings were consistent in both cell line and primary microglia.

Conclusions:

  • NAA reinforces surveillant microglial oxidative metabolism and mitigates inflammatory processes.
  • Reduced NAA levels in neurodegenerative disorders may exacerbate chronic neuroinflammation.
  • NAA holds potential as a therapeutic target for neuroinflammatory conditions.
Keywords:
Anti-inflammatory responseHistone deacetylasesLipid turnoverMicroglial polarizationNAAOxidative metabolism

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