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Related Experiment Video

Updated: Feb 7, 2026

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ACSL1-Dependent Microglial Lipoimmunometabolic Reprogramming Underlies Cognitive Deficits in Alcohol Use Disorder.

Liang Hao1,2, Xing-Rui Cao1,2, Bai-Qiang Li3,4

  • 1Department of Chemistry, School of Forensic Medicine, China Medical University, Shenyang, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
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Summary

Alcohol use disorder (AUD) causes cognitive impairment by altering microglia. Targeting acyl-CoA synthetase long-chain family member 1 (ACSL1) in microglia shows promise for treating these alcohol-related brain deficits.

Keywords:
ACSL1alcohol use disorder (AUD)cognitive deficitslipoimmunometabolic reprogrammingmicroglia

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Alcohol use disorder (AUD) is linked to cognitive impairment, particularly involving prefrontal cortex (PFC) dysfunction.
  • The precise cellular and molecular mechanisms driving this impairment, especially the role of microglia, are not fully understood.

Purpose of the Study:

  • To investigate the role of microglia in AUD-related cognitive deficits.
  • To identify key molecular regulators of microglial dysfunction in AUD.
  • To explore targeted therapeutic strategies for AUD-induced cognitive impairment.

Main Methods:

  • Re-analysis of single-cell RNA sequencing data from AUD patients.
  • Utilized animal and cellular models of chronic ethanol exposure.
  • Investigated acyl-CoA synthetase long-chain family member 1 (ACSL1) and PTPRM signaling pathways.
  • Employed pharmacological inhibition and microglia-specific gene silencing via lipid nanoparticles.

Main Results:

  • Aberrant lipid metabolism pathways and ACSL1 upregulation were identified in microglia from AUD patients and models.
  • Ethanol exposure induced ACSL1-dependent lipid droplet accumulation, neuroinflammation, and altered microglia-neuron interactions.
  • ACSL1 inhibition and microglia-specific silencing ameliorated ethanol-induced cognitive deficits in mice.

Conclusions:

  • ACSL1-mediated reprogramming of microglial lipoimmunity is a key mechanism in AUD-related cognitive impairment.
  • Targeting ACSL1 in microglia represents a novel therapeutic strategy for AUD.