Science Daily today reported that 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 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.
Importantly, these new findings suggest that one of the problems in Parkinson’s disease may be the failure to clear away sick nerve cells with faulty cellular battery packs, to make way for healthy replacements. Instead, sickly and dysfunctional nerve cells may accumulate, which effectively prevents the recruitment of fresh replacements.
Richard G. Carroll, Emilie Hollville, Seamus J. Martin. Parkin Sensitizes toward Apoptosis Induced by Mitochondrial Depolarization through Promoting Degradation of Mcl-1. Cell Reports, 2014; DOI: 10.1016/j.celrep.2014.10.046