The Parkinson disease protein α-synuclein inhibits autophagy.

Abstract

Parkinson disease (PD) is the most common movement disorder affecting people. It is characterized by the accumulation of the protein α-synuclein in Lewy body inclusions in vulnerable neurons. α-Synuclein overexpression caused by gene multiplications is sufficient to cause this disease, suggesting that α-synuclein accumulation is toxic. Here we review our recent study showing that α-synuclein inhibits autophagy. We discuss our mechanistic understanding of this phenomenon and also speculate how a deficiency in autophagy may contribute to a range of pleiotropic features of PD biology.

• Authors: Ashley R Winslow, David C Rubinsztein
• Journal: Autophagy (Autophagy) Vol. 7 Issue 4 Pg. 429-31 (Apr 2011) ISSN: 1554-8635 [Electronic] United States
• PMID: 21157184 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• ATG9B protein, human
• Autophagy-Related Proteins
• Membrane Proteins
• alpha-Synuclein
• rab1 GTP-Binding Proteins

Topics

• Animals
• Autophagy
• Autophagy-Related Proteins
• Gene Expression Regulation
• Golgi Apparatus (metabolism)
• Humans
• Lewy Bodies (metabolism)
• Membrane Proteins (metabolism)
• Mitochondria (metabolism)
• Models, Biological
• Parkinson Disease (metabolism)
• Phagosomes (metabolism)
• alpha-Synuclein (metabolism)
• rab1 GTP-Binding Proteins (metabolism)