Scientists at Trinity College have made an important breakthrough in the medical community’s 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 study is published in the 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. The current study has shown 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.
The laboratory 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.
This discovery is surprising and turns on its head the way researchers thought that Parkin functions. Until now, the medical community have thought of Parkin as a brake on cell death within nerve cells, helping to delay their death. However, the 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.
The team summise that the Parkin protein functions to repair or destroy damaged nerve cells, depending on the degree to which they are damaged. They also state that people living with Parkinson’s disease often have a mutated form of the Parkin gene, which may explain why damaged, dysfunctional nerve cells accumulate.
This work represents a breakthrough in the understanding of how Parkinson’s diseases arises. With this knowledge the researchers hope that the medical community can develop new therapies.
Source: Trinity College Dublin