The catastrophic damage wreaked by a rogue protein involved in Parkinsons’ disease has been tracked by researchers, in work that might help to reinvigorate an old treatment strategy to slow the condition.
A team led by Virginia Lee, a neurobiologist at the University of Pennsylvania in Philadelphia, injected a misfolded synthetic version of the protein α-synuclein into the brains of normal mice and saw the key characteristics of Parkinson’s disease develop and progressively worsen. The study, published today in Science, suggests that the disease is spread from one nerve cell to another by the malformed protein, rather than arising spontaneously in the cells.
The finding raises the possibility that an antibody that binds the misfolded α-synuclein could be used to intercept the protein as it passes between nerve cells. “It’s very hard to ask antibodies not only to get inside the brain, but to get inside cells,” says Lee. “But now you have the possibility of stopping the spreading. And if you stop the spreading, perhaps you can slow the progression of the disease.”
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