New details about a key protein linked to early-onset Parkinson's disease, reported on Thursday in Science, answer many long-standing questions and should aid in development of new treatments, researchers say.
Scientists already knew that in healthy people, the protein called PINK1 senses damage to mitochondria, the energy factories inside of cells. It attaches itself to the damaged mitochondria and tags them so that they can be purged.
When mitochondria are damaged, they stop making energy and release toxins into the cell. In a person with Parkinson's and a PINK1 mutation, damaged mitochondria accumulate in brain cells and the toxins eventually kill the cells.
Researchers also knew that PINK1 mutations cause Parkinson's disease in young adults in particular.
But until now, no one had described the protein's structure, or how it works.
"This is the first time we've seen human PINK1 docked to the surface of damaged mitochondria and it has uncovered a remarkable array of proteins that act as the docking site," study coauthor Dr. Sylvie Callegari of the Walter and Eliza Hall Institute at the University of Melbourne, Australia said in a statement
"We also saw, for the first time, how mutations present in people with Parkinson's disease affect human PINK1," she added.
Seeing what the protein looks like, how it attaches to the mitochondria, and how it is activated "reveals many new ways to change PINK1, essentially switching it on, which will be life-changing for people with Parkinson's," study leader Dr. David Komander, from the same institute, said in a statement.
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