How does Parkinson's disease start and spread? That's a question that many answer with speculation and not a lot of certainty.
What is known: The protein alpha-synuclein builds up in the brain of patients who have the disease, right about when motor dysfunction starts to surface. But do the protein clumps trigger neurodegeneration? Also, how do they spread through the brain? Researchers at the University of Pennsylvania's Perelman School of Medicine believe they figured out the answers by triggering a process that culminated with a Parkinson's-type disease in lab mice. Details are published in the Journal of Experimental Medicine.
In short, they believe the alpha-synuclein protein build-up accelerates the onset of Parkinson's and how bad it gets. They built their theory by injecting "preformed clumps" of human alpha-synuclein into the brains of young mice that were bred to express a mutated form of the protein found in human Parkinson's patients. They first started showing Parkinson's symptoms by one year of age. The finding: The clumps appeared to accelerate the process by luring the mouse version of the alpha-synuclein protein into new clumps. Those in turn spread throughout the brain, from neuron to neuron.
It's an intriguing finding, and suggests, as the researchers note, that Parkinson's may progress like Alzheimer's where unusual amounts of proteins start building up and spreading in the brain. Solving Parkinson's also means figuring out how it operates. But this is a tentative finding that will need to be tested in more preclinical trials before any consistency can be established. Also, mysteries such as what makes the protein clumps start progressing sadly remain unsolved.
- here's the release
- read the journal abstract