A team of scientists discovered a profit that controls the maturity of important neurons in the formation of the cover that covers the nerves, and the study identified a new framework for how the cells control them at the time of their maturity.
This discovery presents a possible approach to renewal medicine to repair the damage caused by sclerosis (multiple sclerosis) and similar diseases that affect the nervous system.
The results show that this brake remains for a very long time in sclerosis, which makes the cells unable to repair the damage caused by the disease.
The study was conducted by researchers from the Institute of Bugs Science at the Faculty of Medicine at the University of “Kis Western Reserve” in the United States, and its results were published in the Cell magazine (CELL) on August 25, and was written by Yurrick Alert.
Poetic sclerosis is classified as autoimmune diseases, and the disease begins with an imbalance in the immune system that accidentally attacks a healthy part of the body.
In sclerosis, the immune system attacks the layer that surrounds and protects the nerves called “myelin sheath”.
“The miles damage causes disability in multiple nervous sclerosis, and the only cells capable of repairing it are the glial cells known as the low -lying cells.”
He added, “By identifying the molecular brake that controls the ripening of low cells, we reveal a clear path to launch the brain repair program,” he added.
How is the miles formed?
The team is now working on the reason for the exacerbation of the state of non -maturity of these cells in the brains of multiple nervous sclerosis, and whether this itself is working in other cells or contributing to stopping the reform in other diseases.
“Multiple nervous sclerosis is a disease that gets worse over time, and patients still lack treatments that restore the miles they have lost. We believe that these new visions will contribute to achieving the promises of renewal treatments that multiple sclerosis needs severely,” Taysar said.
The study focused on low -lying cells that cover neurons with protective miles that are lost in multiple nerve sclerosis.
The low -ingredient cells belong to a category of cells known as the glial cells, which make up more than half of the cells of the nervous system.
And to understand how the low cells acquire their ability to form miles in neurons. Scientists follow thousands of molecular changes during the development of immature cells into a mature, mature cell, and one protein called “S -X6” (SOX6) has emerged.
The team found that the “SOX6” works as a profit, as it stops cells in their immature condition through a phenomenon known as “the melting of genes”.
This brake is essential for proper brain growth, because it prevents the formation of early miles and ensures the maturity of low cells in the appropriate place and time, but in multiple nerve sclerosis it seems that this preventive time mechanism stops.
Gloric cells
For his part, Kevin Alan, co -author of the study from the Faculty of Medicine at the University of “Kis Western Reserve”, said that we were surprised by discovering the ability of the SOX 6 protein to accurately control the maturity of the low cells.
“This provides us with a potential explanation for the inability of these cells often to reinstall the nerve cells damaged in diseases such as multiple sclerosis,” he added.
When the researchers examined the data of the brain tissue in multiple sclerosis patients, they noticed an unusually large number of stuck cells in the event of non -maturity associated with the SOX6 protein, but it seems that this stopping maturity is for multiple sclerosis, and no evidence was found in samples of Alzheimer’s and Parkinson patients.
To test if the release of the brake could accelerate the growth, the team used a target molecular drug called “anti -directional” anti -Xensis “to reduce the SOX6 protein in mice models, and the treated cells have ripened within days and began to form miles of neighboring neurons.
“Our results indicate that the cells are low in multiple sclerosis that do not suffer from a permanent defect, but may simply stop,” said Jesse Zan, co -author of the study from the University of Medicine at the University of “Kis Western Reserve, said.
“And most importantly, we show that it is possible to free these cells from their restrictions to resume their vital functions in the brain,” he added.