Alpha-synuclein's degradation in vivo: Opening a new (cranial) window on the roles of degradation pathways in Parkinson disease

Darius Ebrahimi-Fakhari, Pamela J. McLean, Vivek K. Unni

Research output: Contribution to journalReview article

42 Scopus citations


Progressive accumulation of α-synuclein is key to the pathology of many neurodegenerative diseases, including Parkinson disease and dementia with Lewy bodies. Increased intracellular levels of α-synuclein may be caused by enhanced expression or alterations in protein degradation pathways. Here we review our recent study showing that the ubiquitin-proteasome system and the autophagy-lysosomal pathway are differentially involved in α-synuclein's degradation in vivo. We discuss the key findings obtained with our novel in vivo approach and also present a model for the progression of protein aggregation and dysfunctional degradation in Parkinson disease.

Original languageEnglish (US)
Issue number2
StatePublished - Feb 2012



  • Autophagy
  • Degradation
  • In vivo
  • Lewy bodies
  • Lysosome
  • Multiphoton imaging
  • Neurodegeneration
  • Parkinson disease
  • Proteasome
  • α-synuclein

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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