The accumulation of clumps of the protein, alpha-synuclein, in the brain, in is considered to be the hallmark of Parkinson's disease// , according to Aaron Gitler, a postdoctoral scientist , at the Whitehead Institute in Cambridge, Massachusetts. He, along with fellow postdoctoral researcher, Anil Cashikar, are investigating the ways of preventing formation of these clumps, and also to understand if this might prevent the death of neurons, whose deterioration results in the symptoms of Parkinson’s disease.
They began their work with the simple yeast cells, employing an array engineered by the Harvard Institute of Proteonomics, and infected those cells with alpha-synuclein. They reasoned that if they identified genes that were expressed in a rescued cell, that would alert them about how alpha-synuclein harmed a cell.
Most of the genes they identified were involved in the production of cellular proteins and its folding into the appropriate shape. Working with researchers at the University of Missouri, Kansas City, they demonstrated that a mutated form of alpha-synuclein destroyed a key protein in this process, resulting in cell death.
The next step was to find a gene that could produce this key transport protein, in order to save the cells.
"We were surprised that when we tested this gene in higher animals -- fruit flies, worms, rat cells -- remarkably we could reverse Parkinson's symptoms in higher animals," Gitler said. "There are obvious implications for drug targets and the basic mechanism of how the disease occurs."
The researchers tried various methods of increasing production of the transport protein and in each case; the nerve cells were restored to health.
Their research findings appear in the June 23 issue of the journal Science.
Gitler added. "We hope that in the long run we can get a very good understanding of this and other cellular defects," he said. "Knowing these details will Page: 1 2 Related medicine news :1
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