Researchers have identified a gene that is associated with treatment success in patients with multiple sclerosis being treated with interferon-beta.
A gene for multiple sclerosis (MS) activity has been identified, according to research published in the Annals of Neurology.
Researchers from Brigham and Women’s Hospital examined MS patient disease activity and its link to interferon-beta treatment in order to identify biomarkers for further clinical development and to investigate the pathophysiology of MS disease activity. The researchers wrote that some MS patients experience disease activity despite treatments. Moreover, the authors said, early identification of the most effective drug is important to impacting the long-term outcome for each individual MS patient and improving the personalized approach for treatment.
“This study highlights the fact that genetic variation has a role in the course of a patient’s disease in MS, but that this role is modest and will require much larger studies to be understood in detail,” study author Philip De Jager, MD, PhD, director of the Program in Translational NeuroPsychiatric Genomics at the Ann Romney Center for Neurologic Diseases at BWH explained in a press release. “We need to expand this type of international, collaborative science.”
After screening the genome of MS patients being treated with interferon-beta at the affiliated hospitals of each of the authors (which included Brigham and Women’s, as well as hospitals in Italy and France), the researchers found that the gene that was the most highly indicative of whether or not a patient would respond to treatment was SLC9A9.
“Further work is now needed to validate our results in other collections of patients, particularly patients treated with other MS medications, to evaluate whether the effect of the genetic variant is limited to interferon-beta treatment or is relevant to other clinical MS treatments,” Filippo Martinelli Boneschi, MD, PhD, of San Raffaele Scientific Institute, continued in the statement.
The researchers added that although the role is confirmed in MS, it is weak. The laboratory work in the study demonstrated that the loss of the SLC9A9 gene contributes to immune cells becoming much more likely to initiate damaging immune reactions.
“Manipulations of this gene in mice and in human cells will lead us to better understand mechanisms that are involved in the autoimmune response that causes MS,” added Wassim Elyaman, PhD, an investigator in the Program in Translational NeuroPsychiatric Genomics at the Ann Romney Center for Neurologic Diseases at BWH.