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Lab Research Funded by National MS Society Identifies Possible Target for Promoting Myelin Repair

January 7, 2020

A team at the Mayo Clinic has reported that a eliminating a molecule – called PAR1 – promoted repair of nerve-insulating myelin in mice. FDA-approved therapies exist that block PAR1, and if further research confirms this approach, they could potentially be repurposed to test benefits in people with MS. The team is led by Isobel Scarisbrick, PhD (Mayo Clinic, Rochester, MN).
  • PAR1 is a molecule that is activated by the blood protein thrombin. High levels of thrombin have been found at areas of myelin damage, which is the result of  immune attacks in MS. Thrombin appears to activate PAR1 in areas of myelin damage, preventing myelin repair.
  • In this study, deleting PAR1 in mouse models of myelin damage increased myelin repair. In addition, adding an FDA-approved inhibitor of PAR1 to cells in the laboratory also increased myelin repair.
  • The next step is to test this inhibitor in models of MS to add to evidence that would be needed to evaluate this approach in people with MS.
“Blocking the Thrombin Receptor Promotes Repair of Demyelinated Lesions in the Adult Brain” was published January 7, 2020 in the Journal of Neuroscience.
Read more about research to restore function in MS

About Multiple Sclerosis

Multiple sclerosis is an unpredictable, often disabling disease of the central nervous system. There is currently no cure for MS. Symptoms vary from person to person and range from numbness and tingling, to mobility challenges, blindness and paralysis. An estimated 1 million people live with MS in the United States. Most people are diagnosed between the ages of 20 and 50, and it affects women three times more than men.

About the National Multiple Sclerosis Society

The National MS Society, founded in 1946, funds cutting-edge research, drives change through advocacy, and provides programs and services to help people affected by MS live their best lives. Connect to learn more and get involved:, Facebook, Twitter, Instagram, YouTube or 1-800-344-4867.


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