Medical University Researchers Find New Interaction Linked To Higher Multiple Sclerosis Risk

Researchers from the University of Texas Medical Branch at Galveston and Duke University Medical Center have discovered that people who carry two variants of specific genes have higher chances of developing multiple sclerosis. Their findings are expected to lead to the development of more accurate tests to identify individuals with the greatest risk of the disease.

One of these variants is in IL7R and the other is in DDX39B. The former has already been previously associated with MS while the latter was not known to be connected to the disease until now, MedicalXpress reported.

Aside from leading to more accurate tests for early detection of the disease, the latest discovery could also result to better understanding other autoimmune disorders. The study has been published in the latest issue of "Cell."

Multiple sclerosis is known to be a major cause of neurological disease in younger adults aged 20 to 50 years old. It has also been known to disproportionately affect women.

The disease lets the individual's own immune system attack nerve cells in the spinal cord and brain. MS is treatable but has no cure. It often leads to problems with vision, muscle control, balance, basic body functions, among others, and has the potential to lead to disability.

The study was a collaboration between scientists at UTMB, Duke, University of California, Berkeley, and Case Western Reserve University. They found that when to specific DNA variants in the DDX39B and IL7R genes are present in an individual's genetic code, their interaction could result to an overproduction of the protein sIL7R.

The interactions of this protein with the human body's immune system play a major role in multiple sclerosis. However, its role is still not completely understood.

Lead author Simon Gregory, director of Genomics and Epigenetics at the Duke Molecular Physiology Institute at Duke University Medical Center, said that the study recognizes an interaction between a known MS risk gene to unlock a new MS candidate gene. With this, it opens a new mechanism that is associated with an increased risk of multiple sclerosis as well as other autoimmune diseases.