Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease

ACS Chem Biol. 2006 Aug 22;1(7):420-4. doi: 10.1021/cb600331e.

Abstract

Studies in yeast are providing critical insights into the mechanisms of neurodegeneration in Parkinson's disease (PD). A recent study shows that disruption of vesicular trafficking between the endoplasmic reticulum (ER) and the Golgi, caused by the overexpression and/or aggregation of alpha-synuclein, is linked to degeneration of dopamine neurons. Overexpression of proteins that are known to enhance ER-to-Golgi transport rescue defective trafficking in yeast, worm, fly, and cellular models of PD.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Transport
  • Disease Models, Animal
  • Dopamine / metabolism
  • Endoplasmic Reticulum / metabolism
  • Golgi Apparatus / metabolism
  • Humans
  • Models, Biological
  • Neurodegenerative Diseases / metabolism
  • Neurons / metabolism
  • Oxidative Stress
  • Parkinson Disease / therapy*
  • alpha-Synuclein / toxicity*

Substances

  • alpha-Synuclein
  • Dopamine