New breakthroughs in the research of Parkinson's disease have found scientists identifying a naturally occurring enzyme in the brain. This helps in the destruction of the mutated protein that is the most common cause of inherited Parkinson's disease.
Led by researchers at UT Southwestern Medical Center, the study used human cells and offered a focus for further research into halting the action of the mutated protein.
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Dr. Matthew Goldberg, assistant professor of Neurology and Psychiatry and senior author of the paper said: "There are currently enormous efforts to identify potential therapies based on inhibiting this mutated protein."
He added: "Our paper is a major advance because we identify a protein that binds to the mutated protein and promotes its breakdown."
The particular mutation examined in the study affects a protein whose function is not well understood, but in its normal form, it appears to have multiple sites where other molecules can attach themselves, like a space station with many docking areas.
Named LRRK2, the protein is vulnerable to several mutations, some of which can cause Parkinson's disease.
For the study, the researchers used cultured human kidney cells and found that LRRK2 and a protein called CHIP "robustly" associated with each other.
On further testing, it was found that CHIP and LRRK2 could bind to each other in two different ways, either directly or indirectly by a third molecule that acted as a bridge.
The researchers observed that when CHIP bound to either the normal or mutant form of LRRK2, levels of LRRK2 in the cell decreased. This occurred because the cells increased the rate at which they destroyed LRRK2.
"CHIP may be a useful therapeutic target for treatments to break down LRRK2 in people with Parkinson's," said Goldberg.
He added: "Our next step is to identify cellular mechanisms that signal LRRK2 to be degraded by CHIP or by other mechanisms. Because LRRK2 mutations are believed to cause Parkinsonism by increasing the activity of LRRK2, enhancing the normal mechanisms that target LRRK2 for degradation by CHIP may be therapeutically beneficial."
The study has been published in the journal Public Library of Science.