A recent research by Mayo Clinic has discovered that two genes in mice were associated with good central nervous system repair in multiple sclerosis (MS). Such findings may assist researchers in establishing effectual therapies for treating patients with MS and for identifying MS patients’ outcome.
These two identified genes are expected to be proved as a potential therapeutic target for MS patients. The study has been conducted for examining the main reason pertaining to why some people are infected with MS and others are not.
“Most MS genetic studies have looked at disease susceptibility — or why some people get MS and others do not,” states Allan Bieber, Ph.D., a Mayo Clinic neuroscientist and author of this study. “This study asked, among those who have MS, why do some do well with the disease while others do poorly, and what might be the genetic determinants of this difference in outcome.”
Multiple Sclerosis is known to be an autoimmune disease in which the body’s immune response attacks a person’s central nervous system including areas such as brain, spinal cord and nerves, leading to demyelinating disease. The onset of this disease is generally between the ages of 20 and 40, and is found more common in women. MS is believed to be the most frequent neurological disorder in young adults in North America and Europe.
“It’s possible that the identification of these genes may provide the first important clue as to why some patients with MS do well, while others do not,” explains Dr. Bieber. “The genetic data indicates that good central nervous system repair results from stimulation of one genetic pathway and inhibition of another genetic pathway. While we’re still in the early stages of this research, it could eventually lead to the development of useful therapies that stimulate or inhibit these genetic pathways in patients with MS.”
According to recently conducted data, nearly 330,000 people are diagnosed with MS in the United States. Symptoms include loss of muscle coordination, loss of vigor and strength, debilitated vision, balance and cognition.
“It’s possible that the identification of these genes may provide the first important clue as to why some patients with MS do well, while others do not,” states Dr. Bieber. “The genetic data indicates that good central nervous system repair results from stimulation of one genetic pathway and inhibition of another genetic pathway. While we’re still in the early stages of this research, it could eventually lead to the development of useful therapies that stimulate or inhibit these genetic pathways in patients with MS.”
From the perspective of Dr. Bieber, there may be a small number of powerful genetic determinants for central nervous system repair following demyelinating disease, rather than a larger number of feeble determinants.
“If that’s true, it may be possible to map the most important genetic determinants of central nervous system repair in patients with MS and define a reparative genotype that could predict patients’ outcomes,” comments Moses Rodriguez, M.D., a Mayo Clinic neurologist and director of Mayo Clinic’s Center for Multiple Sclerosis and Central Nervous System Demyelinating Diseases Research and Therapeutics. “Such a diagnostic tool would be a great benefit to patients with MS and is consistent with the concepts of ‘individualized medicine.'”
On the other hand, Dr. Bieber along with a team of Mayo Clinic examiners used two distinct strains of mice with a chronic, progressive MS-like disease. One strain elevated and led to paralysis and death. The other underwent the initial destruction induction phase of the disease and then instantly repaired the damage to the central nervous system and retained most neurological function. By using the strong genetic mapping techniques which are made available for mice, the team mapped two strong genetic determinants of good disease outcome.
This entire conducted research was presented at the Congress of the European Committee for Treatment and Research in Multiple Sclerosis in Dusseldorf, Germany.