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Microglial Ffar4 deficiency promotes cognitive impairment in the context of metabolic syndrome

Wei Wang1, Jinyou Li2, Siyuan Cui3

  • 1Wuxi School of Medicine, Jiangnan University, Wuxi 214000, China.

Science Advances
|February 2, 2024
PubMed

Insights

Free fatty acid receptor 4 (Ffar4) plays a key role in metabolic syndrome (MetS)-related cognitive decline. Targeting Ffar4 in microglia may offer a new therapeutic strategy for preventing dementia associated with MetS.

Area of Science:

  • Neuroscience
  • Metabolic Disorders
  • Immunology

Background:

  • Metabolic syndrome (MetS) is linked to dementia and cognitive impairment.
  • Free fatty acid receptor 4 (Ffar4) may connect genetic and dietary factors in MetS.
  • The specific role of Ffar4 in MetS-associated cognitive dysfunction is not well understood.

Purpose of the Study:

  • To investigate the role of Ffar4 in metabolic syndrome-related cognitive dysfunction.
  • To elucidate the mechanisms by which Ffar4 influences cognitive function in MetS.

Main Methods:

  • Examined Ffar4 expression in MetS mice and patients with cognitive impairment.
  • Utilized conventional and microglial conditional knockout and overexpression of Ffar4 in mice.
  • Investigated the impact of microglial activation, type I interferon signaling, and NF-κB pathway.

Main Results:

  • Ffar4 expression was reduced in MetS mice and patients with cognitive impairment.
  • Ffar4 deficiency in microglia worsened high-fat diet-induced cognitive dysfunction and anxiety.
  • Ffar4 overexpression in microglia ameliorated these deficits, implicating microglial Ffar4 in regulating NF-κB-IFN-β signaling.

Conclusions:

  • Ffar4 negatively regulates microglial activation via the NF-κB-IFN-β pathway.
  • Microglial Ffar4 is crucial for mitigating cognitive decline and anxiety in MetS.
  • Ffar4 presents a potential therapeutic target for delaying MetS-associated cognitive impairment.

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