Parkin protein functions to repair or destroy damaged nerve cells, depending on the degree to which they are damaged. People living with the disease often have a mutated form of Parkin gene. This has been shown by scientists, explaining the possible reason of accumulation of damaged, dysfunctional nerve cells.
Dublin, Ireland, November 13th, 2014 - Scientists at Trinity College Dublin have made an important breakthrough in our understanding of Parkin - a protein that regulates the repair and replacement of nerve cells within the brain. This breakthrough generates a new perspective on how nerve cells die in Parkinson's disease. The Trinity research group, led by Smurfit Professor of Medical Genetics, Professor Seamus Martin, has just published its findings in the internationally renowned, peer-reviewed Cell Press journal, Cell Reports
Although mutation of Parkin has been known to lead to an early onset form of Parkinson's for many years, understanding what it actually did within cells has been difficult to solve. Now, Professor Martin and colleagues have discovered that in response to specific types of cell damage, Parkin can trigger the self-destruction of 'injured' nerve cells by switching on a controlled process of 'cellular suicide' called apoptosis.
Using cutting-edge research techniques, the Martin laboratory, funded by Science Foundation Ireland, found that damage to mitochondria (which function as 'cellular battery packs') activates the Parkin protein, which results in one of two different outcomes - either self-destruction or a repair mode. Which outcome was chosen depended on the degree of damage suffered by the cellular battery packs.