An enzyme that naturally occurs in the brain helps destroy the mutated protein that is the most common cause of inherited Parkinson's disease, researchers at UT Southwestern Medical Center have found.
Their study, using human cells, provides a focus for further research into halting the action of the mutated protein. One of the most famous carriers of the mutation is Google co-founder Sergey Brin, who wrote about it on his blog in 2008.
"There are currently enormous efforts to identify potential therapies based on inhibiting this mutated protein," said Dr. Matthew Goldberg, assistant professor of neurology and psychiatry and senior author of the paper, which appears online in the journal Public Library of Science.
"Our paper is a major advance because we identify a protein that binds to the mutated protein and promotes its breakdown," he said.
The particular mutation that they studied affects a protein whose function is not well understood. In its normal form, it appears to have multiple sites where other molecules can attach themselves, like a space station with many docking areas.
Several mutations can affect the protein, which is named LRRK2. Some of the mutations cause Parkinson's disease.
The current theory is that the mutation leads to increased function of LRRK2 and to the formation of abnormal clumps of proteins inside brain nerve cells. The cells eventually die from these effects.
In the current study, the researchers used cultured human kidney cells and found that LRRK2 and a protein called CHIP "robustly" associated with each other.