We’ve all heard about Parkinson’s disease, and the devastation that is associated with it. But what is Parkinson’s disease? What does it imply? Parkinson’s disease is a progressive disorder of the nervous system; developing gradually, it can begin with something as simple as a hand tremor, and eventually progress to stiffening and/or slowing of movement. Although there exist many remedies to extend one’s life, there does not exist a single cure to the malady.
Much of the reason for why there is no cure to Parkinson’s disease is our limited understanding of the disease; it is a complex disorder, and until now it has proved difficult to decrypt and comprehend. However, scientists at the Trinity College Dublin, led by Professor of Medical Genetics Seamus Martin, have made a significant breakthrough in our understanding of Parkin, a protein that regulates the repair and replacement of nerve cells in the brain. This generates a different perspective on the behavior of nerve cells during the course of Parkinson’s disease.
Although the association between a mutation in Parkin and early onset of Parkinson’s disease has long been known, an actual understanding of the effect of mutated Parkin within cells was unknown to scientists. Utilizing research techniques funded by Science Foundation Ireland, the Martin Laboratory found that damage to the mitochondria (the main source of energy in cells) activates the Parkin protein. The activation of this protein results in one of two outcomes: apoptosis or cell “repair” mode, depending on the severity of the damage to the cell. Martin said his team discovered that Parkin has a destruction mechanism whereby it can “identify when cells are past their sell-by date and get rid of them”.
Parkin has the ability to decipher whether a cell has sustained enough mitochondrial damage to commit “cellular suicide” through apoptosis or be repaired. However, mutated Parkin cannot trigger apoptosis in cells, resulting in the accumulation of dysfunctional cells.
Image Source: Andrew Brookes
Professor Seamus Martin believes that this discovery could be extremely significant in understanding the relationship between mutated Parkin proteins and early onset Parkinson’s disease. Martin asserts that one of the problems with Parkinson’s is the body’s inability to rid itself naturally of cells that have past their “expiration dates.” Because the Parkin protein regulates whether or not cells undergo apoptosis and because of the existing relationship between a mutation in the protein and having Parkinson’s, Martin is optimistic that these discoveries cannot be pure coincidences. He concludes that the accumulation of sickly cells inhibits the production of fresh healthy cells to replace the sick ones. In a body with healthy Parkin proteins, the body is able to rid of “injured” cells that have mitochondrial damage, making room for the production of new, healthy cells. A mutation in the Parkin protein, however, prevents natural cell death through the controlled process of apoptosis, thereby leading to an accumulation of cells with mitochondrial damage. Further, one of the known effects of Parkinson’s disease on an anatomical level is the accumulation of damaged, dysfunctional nerve cells.
Naturally, therefore, Martin was extremely excited about this newfound discovery, commenting: “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 is sure that this breakthrough, at the very least, is a step in the right direction to figuring out how Parkinson’s disease operates, and, ultimately, a cure.
Feature Image Source: Eu Sou by jeronimo sanz