While inflammation often causes damage to the nerves of multiple sclerosis (MS) patients, a group of HBI researchers has been studying how neuroinflammation can instead be harnessed to repair the damage caused by this disease.

Dr. V.W. Yong’s laboratory set out to test whether a drug that is used to treat MS symptoms, Copaxone or glatiramer acetate (GA), could also play a role in repairing the covering of nerves that have been damaged by MS.  

“We know the drug is safely used around the world but we wanted to know if GA offered any reparative benefits,” said Claudia Silva, laboratory manager for the Yong lab.

In MS, axons (the wiring between cells) lose their protective covering, otherwise known as myelin. The myelin helps nerve cells transmit signals and without it axons cannot carry information as quickly or efficiently, which can lead to the short or jerky movements demonstrated by some MS patients.

Yong’s team attempted to enhance the body’s ability to re-cover axons with myelin, by stimulating cells in the immune system to produce beneficial growth factors.  The researchers isolated a specific immune cell, the TH2 helper cell, and found that GA caused these TH2 cells to secrete several growth factors. Those growth factors in turn caused cells in the nervous system that are responsible for making myelin, oligodendrocytes, to grow.  

In various models of MS, the team saw that the application of GA led to an increase in both the number of new oligodendrocytes being created and to positive indicators that damaged nerves were being remyelinated.  


“Our study demonstrated a neuronal repair capacity induced by glatiramer acetate therapy, further extending both an anti-inflammatory and neuroprotective mechanism associated with this treatment, and suggesting that long-term benefits of GA in MS patients may be, in part, due to remyelination,” said Dr. Yong. 

The results of this work were published this week in the
Proceedings of the National Academy of Sciences(PNAS), one of the world’s most-cited scientific journals.  HBI members Drs. Sam Weiss, Andrew Chojnacki and Axinia Döring also contributed to the project, along with Dr. Viktor Skihar, a former postdoctoral fellow in Dr. Yong’s laboratory who recently finished his training at the HBI and has returned to the University of Saskatchewan. 

Further research and clinical trials could lead to an understanding that GA can not only treat the symptoms of MS for patients but that it may also provide protection or repair for the nerve damage caused by this devastating disorder.