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Parkinson's disease mechanism discovered

Howard Hughes Medical Institute researchers have pinpointed defects in a critical cellular pathway that can lead to the death of dopamine-producing nerve cells and ultimately Parkinson's symptoms. Their studies have also identified a new way to rescue dying neurons in several animal models of Parkinson's disease.

According to the researchers, the findings offer a promising opportunity for developing new drugs to treat the underlying causes of Parkinson's disease and related neurodegenerative disorders.

The research team, which included Howard Hughes Medical Institute investigators Susan L. Lindquist and Nancy M. Bonini, published their findings on June 22, 2006, in Science Express, which provides electronic publication of selected Science papers in advance of print. Lindquist is at the Whitehead Institute for Biomedical Research and Bonini is at the University of Pennsylvania. Antony Cooper of the University of Missouri-Kansas City and Aaron Gitler, who is in Lindquist's laboratory, were co-lead authors on the paper. Other co-authors were from Purdue University, the University of Alabama, Medical College of Georgia and New York University.

The researchers' began their experiments seeking to clarify the role of the protein alpha-synuclein in Parkinson's disease. It had long been known that abnormalities in alpha-synuclein could cause a lethal buildup of the protein in neurons. Researchers also knew that accumulation of alpha-synuclein caused neurodegeneration in animal models of Parkinson's disease, but little was known about alpha-synuclein's normal cellular function or how it contributed to disease. One major problem facing researchers, Lindquist said, was that alpha-synuclein accumulation causes a range of abnormalities, and it was not possible to sort out which were causes and which were effects in Parkinson's disease pathology.

However, Lindquist's team developed a technique to switch on overproduction of alpha-synuclein in yeast,
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Source:Howard Hughes Medical Institute


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