Millipore Home

• Home
• Products
• Services
• Learning Center
• Tech Library
• Support
• Company

Product Reference

Increased glutathione S-transferase activity rescues dopaminergic neuron loss in a Drosophila model of Parkinson's disease.

Author	Alexander J Whitworth, Dorothy A Theodore, Jessica C Greene, Helen Benes, Paul D Wes, Leo J Pallanck
Citation Information	Proceedings of the National Academy of Sciences of the United States of America, 102:8024-9 (2005)
Keywords	Animals, Drosophila, Drosophila Proteins, Gene Expression, Glutathione Transferase, Green Fluorescent Proteins, Interneurons, Locomotion, Microscopy, Confocal, Mutation, Nerve Degeneration, Parkinson Disease
Related Products	AB152
Pub Med ID	15911761

Loss-of-function mutations of the parkin gene are a major cause of early-onset parkinsonism. To explore the mechanism by which loss of parkin function results in neurodegeneration, we are using a genetic approach in Drosophila. Here, we show that Drosophila parkin mutants display degeneration of a subset of dopaminergic (DA) neurons in the brain. The neurodegenerative phenotype of parkin mutants is enhanced by loss-of-function mutations of the glutathione S-transferase S1 (GstS1) gene, which were identified in an unbiased genetic screen for genes that modify parkin phenotypes. Furthermore, overexpression of GstS1 in DA neurons suppresses neurodegeneration in parkin mutants. Given the previous evidence for altered glutathione metabolism and oxidative stress in sporadic Parkinson's disease (PD), these data suggest that the mechanism of DA neuron loss in Drosophila parkin mutants is similar to the mechanisms underlying sporadic PD. Moreover, these findings identify a potential therapeutic approach in treating PD.