Maya Brinster
“Molecular Switch for Repairing Central Nervous System Disorders.” ScienceDaily,
ScienceDaily, 10 Jan. 2020, https://www.sciencedaily.com/releases/2020/01/200110111531.ht
For current event #5, I read the article “Molecular switch for repairing central nervous system disorders.” It describes an exciting study conducted by Mayo Clinic researchers that found a new strategy for treating central nervous system disorders. Many of these disorders, such as multiple sclerosis, Alzheimer’s, and schizophrenia, are caused by the injury of myelin. Myelin acts as an insulator around nerves, protecting electrical signals that flow through the nervous system. It is extremely important for the nervous system to function properly, and Myelin deterioration can lead to loss of sensory and motor function. The PAR1 receptor will block myelin production and lead to this deterioration. A certain protein in blood that helps with healing, called thrombin, will trigger that receptor and subsequently block the production of myelin. Blocking the PAR1 receptor will lead to the regeneration of myelin. By testing two mice, both of which suffered from disorders caused by myelin deterioration, researchers at the Mayo Clinic discovered a way to genetically block PAR1 and also found that a certain drug approved by the Food and Drug Administration was able to improve myelin production and inhibit PAR1 in cell samples as well. Although this drug proved to be successful in isolated cells, scientists are unsure of the effects on animals, and therefore do not recommend that patients take the drug until further research is conducted. Dr. Scarisbrick, a researcher at the Mayo Clinic, explains, “We have not used the drug in animals yet, and it is not ready to put in patients for the purpose of myelin repair.”
Although this inhibitor is not ready for human consumption, it is still an incredible step forwards in the medical field and has the potential to reverse the effects of these devastating diseases. This article has made me much more optimistic about the future of these diseases, and hopefully, years from now, they won’t be as prominent of issues as they are now.
The authors of this article did a great job explaining both the causes and effects of myelin deterioration, as well as the significance of the PAR1 receptor. This background information that they thoroughly explained is vital in the understanding of the article as a whole. However, the authors were rather unclear about the specific findings of the researchers. They stated that researchers found a way to genetically block PAR1, but never elaborated on this point. Instead, they switched to an entirely different PAR1 inhibitor drug that could also lead to myelin regeneration. This was pretty confusing, and I wish I could’ve read more about how they genetically blocked the PAR1 and whether it can possibly be used in humans, not just mice. In the future, it would be helpful for the authors to elaborate on all information they explained instead of simply stating a finding and moving on. Overall, however, this was a very interesting article and I’m glad that I chose to read it.