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VPS35 and retromer dysfunction in Parkinson's disease.

Jordan Rowlands1, Darren J Moore1

  • 1Department of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI 49503, USA.

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|February 18, 2024
PubMed
Summary

Mutations in the vacuolar protein sorting 35 ortholog (VPS35) gene cause Parkinson's disease by disrupting endosomal recycling. Understanding VPS35 dysfunction offers insights into neurodegeneration and potential therapeutics.

Keywords:
Parkinson's disease (PD)VPS35endosomelysosomeretromervesicular sorting

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Area of Science:

  • Neuroscience
  • Genetics
  • Cell Biology

Background:

  • The vacuolar protein sorting 35 ortholog (VPS35) is crucial for the retromer complex, essential for endosomal cargo recycling.
  • Deficits in the endo-lysosomal pathway are implicated in neurodegenerative diseases like Parkinson's disease (PD).
  • VPS35 mutations, particularly D620N, are linked to autosomal dominant, late-onset PD.

Purpose of the Study:

  • To review current knowledge on VPS35 and its role in PD pathogenesis.
  • To discuss mechanisms of VPS35-mediated neurodegeneration and its interplay with other PD-linked genes.
  • To explore how VPS35 dysfunction provides insights into sporadic PD.

Main Methods:

  • Literature review focusing on VPS35 function, mutations, and PD.
  • Analysis of cellular and animal models with VPS35 mutations.
  • Discussion of the interplay between VPS35 and other PD-associated genetic factors.

Main Results:

  • The PD-linked D620N VPS35 mutation impairs retromer function and WASH complex recruitment.
  • VPS35 dysfunction is associated with LRRK2 hyperactivation, mitochondrial issues, and autophagy-lysosomal deficits.
  • Altered neurotransmitter receptor transport is observed in VPS35-linked PD models.

Conclusions:

  • VPS35 is a key player in PD pathogenesis, with mutations leading to neurodegeneration via multiple cellular pathways.
  • Studying VPS35 D620N provides a model for understanding sporadic PD.
  • Targeting VPS35-related pathways may offer therapeutic strategies for Parkinson's disease.