Grand Rapids, Mich. (June 27, 2012) Van Andel Institute announces that researchers at Lund University in Sweden have published a study detailing how Parkinson's disease spreads through the brain. Experiments in rat models uncover a process previously used to explain mad cow disease, in which misfolded proteins travel from sick to healthy cells. This model has never before been identified so clearly in a living organism, and the breakthrough brings researchers one step closer to a disease-modifying drug for Parkinson's.
"Parkinson's is the second most common neurodegenerative disorder after Alzheimer's disease," said Patrik Brundin M.D., Ph.D., Jay Van Andel Endowed Chair in Parkinson's Research at Van Andel Research Institute (VARI), Head of the Neuronal Survival Unit at Lund University and senior author of the study. "A major unmet medical need is a therapy that slows disease progression. We aim to better understand how Parkinson's pathology progresses and thereby uncover novel molecular targets for disease-modifying treatments."
Previous research demonstrates that a misfolded protein known as alpha-synuclein protein gradually appears in healthy young neurons transplanted to the brains of Parkinson's patients. This discovery gave rise to the group's hypothesis of cell-to-cell protein transfer, which has since been demonstrated in laboratory experiments.
In the current study, published this week in the PLoS ONE, researchers for the first time were able to follow events in the recipient cell as it accepts the diseased protein by allowing it to pass its outer cell membrane. The experiments also show how the transferred proteins attract proteins in the host cell leading to abnormal folding or "clumping" inside the cells.
"This is a cellular process likely to lead to the disease process as Parkinson's progresses, and it spreads to an increasing number of brain regions as the patient gets sicker," said Elodie Angot, Ph.D., of Lu
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Van Andel Research Institute