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Related Experiment Video

Updated: Mar 29, 2026

Assessing Functional Performance in the Mdx Mouse Model
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Anti-Inflammatory and Synaptic Protective Effects of TNF-α Inactivation in the MDX Mouse Model.

Anna Oller Bonani1, Valquíria Matheus2, Ana Laura Midori Rossi Tomiyama1

  • 1Laboratory of Nerve Regeneration, Department of Structural and Functional Biology, Institute of Biology, UNICAMP, Campinas 13083-862, SP, Brazil.

Current Issues in Molecular Biology
|March 28, 2026
PubMed
Summary

Etanercept treatment reduced inflammation and improved motor function in Duchenne muscular dystrophy (DMD) mouse models. This TNF-α blockade offers potential neuroprotective benefits for DMD patients.

Keywords:
Duchenne muscular dystrophyMDXcentral nervous systemspinal motoneuronssynapsetumor necrosis factor alpha

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Duchenne muscular dystrophy (DMD) involves muscle degeneration and central nervous system alterations due to lack of dystrophin.
  • Sustained inflammation and glial activation, particularly TNF-α, exacerbate muscle fiber damage in DMD.
  • MDX mice serve as a model for studying DMD pathology and potential treatments.

Purpose of the Study:

  • To investigate the anti-inflammatory and neuroprotective effects of Etanercept, a TNF-α inhibitor.
  • To assess Etanercept's impact on the spinal cord of MDX mice, a DMD model.
  • To evaluate Etanercept's influence on neuroinflammation and locomotor function.

Main Methods:

  • MDX and control mice received vehicle or Etanercept (3, 6, or 12 mg/Kg) intraperitoneally every 72 hours for two weeks.
  • Daily gait assessments were conducted to monitor locomotor function.
  • Flow cytometry and immunolabeling analyses were performed on lumbar spinal cord tissue.

Main Results:

  • Etanercept (12 mg/Kg) significantly reduced astrogliosis and microglial activation in MDX mice.
  • Treatment restored synaptic markers (synaptophysin, GAD-65, VGLUT-1) and decreased pro-inflammatory cytokines.
  • Etanercept decreased GFAP+/TNF-α+ astrocytes, downregulated Th1 lymphocyte polarization, and improved locomotor function.

Conclusions:

  • TNF-α blockade by Etanercept demonstrates significant neuroprotective and anti-inflammatory effects in the spinal cord of dystrophic mice.
  • These findings highlight the critical role of TNF-α signaling in DMD-associated neuroinflammation.
  • Etanercept presents a potential therapeutic strategy for mitigating central nervous system complications in DMD.