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DNAJB6b-enriched small extracellular vesicles decrease polyglutamine aggregation in in vitro and in vivo models of

Bhagyashree S Joshi1, Sameh A Youssef2,3, Reinier Bron1

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Neural stem cell-derived extracellular vesicles efficiently deliver DNAJB6 to the brain, reducing toxic protein aggregation in Huntington disease models and mice.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Huntington disease (HD) is a neurodegenerative disorder caused by expanded polyglutamine (polyQ) in the huntingtin (HTT) protein, leading to aggregation.
  • DNAJB6, a DNAJ chaperone, effectively inhibits polyQ aggregation in various models.
  • Efficient delivery of DNAJB6 to the brain is crucial for therapeutic intervention in HD.

Purpose of the Study:

  • To evaluate neural stem cell-derived small extracellular vesicles (sEVs) as a delivery system for DNAJB6 in Huntington disease.
  • To assess the efficacy of DNAJB6-loaded sEVs in reducing mutant HTT aggregation in cellular and animal models of HD.

Main Methods:

  • Small extracellular vesicles (sEVs) were derived from neural stem cells (NSCs).
  • sEVs were engineered to overexpress DNAJB6.
  • DNAJB6-enriched sEVs were administered to cells with expanded polyQ tracts and injected intrathecally into R6/2 transgenic HD mice.

Main Results:

  • Administration of DNAJB6-overexpressing sEVs suppressed HTT aggregation in cells.
  • Intrathecal injection of DNAJB6-enriched sEVs significantly reduced mutant HTT aggregation in the brains of HD mice.
  • sEVs demonstrated potential for protecting DNAJB6 from degradation and facilitating brain penetration.

Conclusions:

  • sEV-mediated delivery of DNAJB6 shows promise as a therapeutic strategy for Huntington disease.
  • This approach may help delay disease onset by reducing toxic protein aggregation in the brain.
  • Further research into sEV-based chaperone delivery could offer new avenues for treating neurodegenerative disorders.