Rescuing Defective Vesicular Trafficking Protects against α-Synuclein Toxicity in Cellular and Animal Models of Parkinson’s Disease
- 1 August 2006
- journal article
- review article
- Published by American Chemical Society (ACS) in ACS Chemical Biology
- Vol. 1 (7) , 420-424
- https://doi.org/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 α-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.Keywords
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