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Damaged Proteins May Travel from Cell to Cell, Spreading Parkinsonís in the Brain
- Jan 28 2011
A new study suggests that a damaged protein can spread from sick cells to healthy ones in the brain, providing a possible explanation for how Parkinson’s disease (PD) progresses. The study appears in the January 19 online edition of the Journal of Clinical Investigation.
In people with Parkinson’s, neurons, nerve cells in the brain that help control the body’s movements, develop clusters of the protein alpha-synuclein. When these proteins clump, they are known as Lewy bodies, and have been linked to the cell death responsible for PD. In earlier research, two separate teams: one led by Patrik Brundin, Ph.D., M.D., at Lund University in Sweden and the other led by Jeffrey Kordower, Ph.D., at the Parkinson’s Disease Foundation (PDF) Center for Parkinson’s Research at Rush University in Chicago, studied the brains of people with Parkinson’s who had received transplants of healthy young neurons as a therapy. Both teams found that the newly transplanted neurons also developed Lewy bodies. This suggested that the new transplanted neurons “contracted” PD from the brain in which they were transplanted.
In the new study, Dr. Brundin and colleagues tested the idea that alpha-synuclein can travel from one cell to another. First, he and his team studied the process in cell culture—that is, in nerve cells grown in the laboratory. Then they carried out experiments in mice with PD symptoms and excess alpha-synuclein in their brains. The researchers transplanted healthy neurons into the brains of these mice and observed their effects.
- Laboratory experiments demonstrated that the alpha-synuclein protein can indeed move from one neuron to another in both cell culture and in living animals.
- The scientists were able to use chemicals to block the spread of alpha-synuclein, suggesting a mechanism by which the alpha-synuclein travels from one neuron to another.
- Alpha-synuclein that entered healthy neurons could initiate or "seed" the formation of these Lewy body clumps.
What Does it Mean?
This study aimed to assess the “contagious protein” hypothesis of Parkinson’s disease, which theorizes that neurons may “infect” other neurons with damaged alpha-synuclein, a protein which is very important in the pathogenesis of PD. In 1997, Stanley Pruziner, M.D., received the Nobel Prize for his surprising discovery that some damaged proteins, rather than live organisms such as bacteria or viruses, can be infectious. Damaged or mis-folded proteins have since been implicated in mad cow disease, Creutzfeldt-Jakob disease and other brain disorders. The study demonstrates that the protein alpha-synuclein is able to enter and affect healthy neurons. The protein may also initiate the formation of new Lewy body clumps which are the hallmark of Parkinson’s disease.
Much about the nature of the alpha-synuclein “seeding” remains unclear. Additional research is required to assess whether the alpha-synuclein “infectivity” is the cause of PD disease progression or is simply a minor aspect of the disease itself. Lastly, these results – if confirmed – lend support to potential new therapies aimed at stopping, reducing or delaying the spread of the toxic form of alpha-synuclein. Simply put: knowing how the disease spreads may help stop it altogether.
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Reference: α-Synuclein propagates from mouse brain to grafted dopaminergic neurons and seeds aggregation in cultured human cells. Hansen C, Angot E, Bergström AL, Steiner JA, Pieri L, Paul G, Outeiro TF, Melki R, Kallunki P, Fog K, Li JY, Brundin P. J Clin Invest. 2011 Jan 18. pii: 43366. doi: 10.1172/JCI43366. [Epub ahead of print] (http://www.ncbi.nlm.nih.gov/pubmed/21245577).
Source Date: Jan 28 2011