Abstract
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 language | English (US) |
---|---|
Journal | Autophagy |
Volume | 8 |
Issue number | 2 |
State | Published - Feb 2012 |
Keywords
- Autophagy
- Degradation
- In vivo
- Lewy bodies
- Lysosome
- Multiphoton imaging
- Neurodegeneration
- Parkinson disease
- Proteasome
- α-synuclein
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology