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VPS35 and the mitochondria: Connecting the dots in Parkinson's disease pathophysiology

Gianni Cutillo1, David K Simon1, Simona Eleuteri1

  • 1Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, MA 02215, USA.

Neurobiology of Disease
|August 28, 2020
PubMed

Insights

Mutations in VPS35 (retromer component) are linked to Parkinson's disease (PD). This review explores VPS35's role in mitochondrial health and its potential as a neuroprotective target for PD.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Mutations in VPS35 (retromer component) are a rare cause of autosomal dominant Parkinson's disease (PD).
  • VPS35 is essential for endosomal trafficking, but emerging evidence implicates it in mitochondrial dynamics and homeostasis.
  • Parkinson's disease is a common neurodegenerative disorder with complex pathological mechanisms.

Purpose of the Study:

  • To review the intricate relationship between VPS35 and mitochondria.
  • To highlight the potential significance of this crosstalk in Parkinson's disease pathogenesis.
  • To explore VPS35 as a potential therapeutic target for PD.

Main Methods:

  • Literature review of studies investigating VPS35 function.
  • Analysis of genetic links between VPS35 mutations and PD.
  • Examination of VPS35's role in α-synuclein pathways and mitochondrial stability.

Main Results:

  • VPS35 plays a critical role in maintaining mitochondrial stability and function.
  • VPS35 is involved in pathways related to α-synuclein accumulation and clearance.
  • Dysregulation of VPS35 impacts cellular processes relevant to PD.

Conclusions:

  • The interplay between VPS35 and mitochondria is crucial for cellular homeostasis.
  • Targeting VPS35 may offer a novel neuroprotective strategy for Parkinson's disease.
  • Further research into VPS35's mitochondrial functions could elucidate PD mechanisms.
Keywords:
Endosomal traffickingMitochondrial dynamicNeuroprotectionParkinson's diseaseTherapeutic approachVPS35

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