The brains of patients with Parkinson's disease are riddled with clumps of misfolded α-synuclein protein, which is normally soluble in brain cells. Virginia Lee and her colleagues at the University of Pennsylvania in Philadelphia show that synthetic fibrils of this protein can enter mouse neurons unassisted and convert normal α-synuclein into the insoluble aggregates seen in human brains.
Two weeks after mixing the fibrils with the neurons, the authors observed an increase in insoluble clumps and a decrease in normal α-synuclein in the cells. The clumps spread throughout the neurons, impairing their ability to form connections. Cell death was 68% higher in treated cells than in control neurons.
The findings suggest a mechanism for how neurodegeneration can 'spread' throughout the brain.
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Parkinson's propagator. Nature 478, 158 (2011). https://doi.org/10.1038/478158b
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DOI: https://doi.org/10.1038/478158b
