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Targeting senescent microglia in progressive multiple sclerosis: a geroscience-informed approach.

Jeffrey Atkinson1,2, Amy Dokiburra2, Hayley Groover2,3

  • 1Department of Neurology, The Ohio State University College of Medicine, Wexner Medical Center, Columbus, OH, United States.

Frontiers in Immunology
|October 23, 2025
PubMed
Summary
This summary is machine-generated.

Cellular senescence contributes to progressive multiple sclerosis (MS) by promoting inflammation and neurodegeneration. Senolytic therapies, targeting senescent cells, show promise in reducing MS disease severity and improving outcomes.

Keywords:
agingexperimental autoimmue encephalomyelitisgerosciencemultiple sclerosissenolytic

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Area of Science:

  • Neuroimmunology
  • Geroscience
  • Neurodegenerative Diseases

Background:

  • Multiple sclerosis (MS) is a CNS disorder characterized by neuroinflammation and neurodegeneration, with age increasing disease severity.
  • Cellular senescence, marked by a pro-inflammatory senescence-associated secretory phenotype (SASP), exacerbates tissue injury and is implicated in MS pathogenesis.
  • Senescent microglia within MS lesions may impair remyelination and worsen neurodegeneration, creating a detrimental cycle.

Purpose of the Study:

  • To investigate the therapeutic potential of senolytic agents in a mouse model of MS.
  • To determine if targeting cellular senescence can ameliorate disease progression and improve outcomes in experimental autoimmune encephalomyelitis (EAE).

Main Methods:

  • Utilized experimental autoimmune encephalomyelitis (EAE), a model for MS, in middle-aged mice.
  • Administered senolytic drugs, dasatinib plus quercetin (D+Q) or navitoclax, to EAE mice.
  • Assessed clinical outcomes, survival rates, and senescent cell burden.

Main Results:

  • Senolytic treatment with D+Q or navitoclax significantly improved clinical outcomes and survival in middle-aged EAE mice.
  • Treatment reduced the burden of senescent microglia in the central nervous system (CNS).
  • Results demonstrate an age- and drug-dependent attenuation of EAE severity.

Conclusions:

  • Senolytic therapy is a promising geroscience-based strategy for progressive MS.
  • Targeting cellular senescence may offer a novel therapeutic approach for neuroinflammatory and neurodegenerative conditions.
  • Further research is needed to translate senolytic therapy to human MS clinical applications.