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Microglial STING is a central safeguard against neurological decline with age

Katherine B Sulka1, Kimberly A Carroll1, Machlan Sawden1

  • 1Department of Immunology, Tufts University School of Medicine, Boston, MA 02111, USA; Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA.

Cell Reports
|June 1, 2025
PubMed

Insights

The stimulator of interferon genes (STING) pathway protects the aging brain. STING deficiency worsens neurological decline by increasing blood-brain barrier breakdown and DNA damage in aged mice.

Area of Science:

  • Neuroscience
  • Immunology
  • Aging Research

Background:

  • Functional decline in the central nervous system (CNS) is linked to blood-brain barrier (BBB) breakdown and inflammation, common in neurodegeneration.
  • The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway's role in physiological brain aging is not well understood.

Purpose of the Study:

  • To investigate the role of the STING pathway in maintaining CNS function during physiological aging.
  • To determine the impact of STING deficiency on age-related neurodegeneration and associated molecular changes.

Main Methods:

  • Utilized physiologically aged mice to study the effects of STING deficiency on CNS function.
  • Assessed neurological decline, BBB integrity, microhemorrhages, and neuromotor deficits.
  • Analyzed neuronal DNA damage, CNS inflammatory profiles, type I interferon responses, and senescence markers.

Main Results:

  • STING deficiency exacerbated neurological decline, characterized by BBB breakdown, microhemorrhages, and impaired neuromotor function in aged mice.
  • Loss of STING led to increased neuronal DNA damage and altered CNS inflammatory, type I interferon, and senescence signatures.
  • Microglial phenotypes and transcriptomes were significantly altered in STING-deficient aged mice.

Conclusions:

  • STING plays a vital, protective role in preserving CNS function during physiological aging.
  • Microglial STING expression is sufficient to confer protection against age-associated CNS changes.
  • This study elucidates the mechanistic basis for STING-dependent neuroprotection in the aging brain.
Keywords:
CNSCP: ImmunologyCP: NeuroscienceDNA damageSTINGagingblood-brain barrierinflammationinnate immunitymicroglianeuro-motor dysfunctionsenescencetype 1 interferons

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