帕金森 z-bo 2020-10-19 327

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

　　The findings of the team have been published in Celleports. It is well known that mutations in Parkinson's protein can cause early onset of Parkinson's disease, but it is difficult to explain its mechanism of action in cells. Martin and his colleagues discovered that Parkin, in response to certain types of cell damage, self-destructs "damaged" nerve cells by initiating a "cell suicide" (called apoptosis) process. I found this may cause.

　　Researchers used the most advanced technology to find that damaged mitochondria activated Perkin. This leads to two different results: "damaged" nerve cells destroy themselves or enter repair mode. The choice of results depends on the degree of damage to cell mitochondria. Importantly, these new findings indicate that one of the problems with Parkinson's disease may be the inability to remove nerve cells with abnormal mitochondrial function. On the contrary, weak, diseased and abnormal nerve cells will accumulate and effectively prevent nerve cell replacement.

　　Professor Martin commented on these findings and said: This discovery is amazing. We believe that Perkin acts as a brake mechanism for nerve cell death and helps delay nerve cell death. But new data shows that the opposite is true. Perkin can actually help get rid of injured "sick" nerve cells, which can promote their replacement, which suggests that Parkinson's disease may be caused by the failure of the clearance process and the accumulation of defective neurons.