帕金森氏病 z-bo 2020-09-17 340

　　Scientists at Trinity College Dublin have made significant progress in understanding Parkin protein, which regulates the maintenance and replacement of nerve cells in the brain. This breakthrough discovery provides a new perspective on how nerve cells die in Parkinson's disease.

　　team's research results have been published in Celleports. It is well known that mutations in Parkinson's protein can cause early onset of Parkinson's disease, but its mechanism of action in cells is still difficult to explain. Currently, Professor Martin and his colleagues initiate the process of "cell suicide" (called apoptosis) in response to certain types of cell damage to induce "injured" nerve cells to self-destruct. I found that I can do it. Researchers used the most advanced technology to find that damaged mitochondria activate Parkinson's bacteria, leading to two different consequences: the self-destruction of "damaged" nerve cells or the activation of a repair mode. Find. The choice of outcome depends on the degree of damage suffered by the cell mitochondria. Importantly, these new findings indicate that one of the problems with Parkinson's disease may be the inability to eliminate nerve cells due to mitochondrial dysfunction. On the contrary, fragile and sick abnormal nerve cells will accumulate and effectively prevent nerve cell replacement.

　　Professor Martin commented on this discovery and said: This discovery is surprising. We believe that Perkin can act as a brake mechanism for nerve cell death and help delay nerve cell death.

　　But the new data is the opposite: Perkin actually helps get rid of injured "sick" nerve cells, which may help their replacement. This suggests that Parkinson's disease may be caused by the failure of the clearance process and the accumulation of defective neurons.