Parkin-expressing cells
(red) are undergoing programmed cell death. Credit: Dr Emilie Hollville and
Professor Seamus Martin, Trinity College Dublin
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.
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.
Commenting on the
findings, Professor Martin stated: "This discovery is surprising and turns
on its head the way we thought that Parkin functions. Until now, we have
thought of Parkin as a brake on cell death within nerve cells, helping to delay
their death. However, our new data suggests the contrary: Parkin may in fact
help to weed out injured and sick nerve cells, which probably facilitates their
replacement. This suggests that Parkinson's disease could result from the
accumulation of defective neurons due to the failure of this cellular weeding
process."
Professor Martin also
added: "We are very grateful for the support of Science Foundation
Ireland, who funded this research. This work represents an excellent example of
how basic research leads to fundamental breakthroughs in our understanding of
how diseases arise. Without such knowledge, it would be very difficult to
develop new therapies."
Parkin-expressing cells (red) are undergoing programmed cell death.
Credit: Dr Emilie Hollville and Professor Seamus Martin, Trinity College Dublin
http://health.einnews.com/article/234538918/v-AWr8PJ31SOWdCT?n=2&code=ga_qGBxHZ2aVYO4P
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