Protein Shows Promise in Treatment of Spinal Cord Injuries


By Kevin Ritchart

It’s estimated that more than a quarter of a million people in the U.S. are living with spinal cord injuries, with 12,000 Americans suffering new injuries each year. While improved emergency care, more potent antibiotics and aggressive rehabilitation regimens can serve to minimize nervous system damage and restore function to some degree, those who have not experienced positive results from these modes of treatment are still in search of treatments that will aid them in their quest to restore functional movement.

Evolving surgical techniques, developments in spinal nerve regeneration, cell replacement, neuroprotection and neurorehabilitation – along with new research – provide hope that the future of spinal cord injury treatment will continue to advance and improve the lives of those living with these injuries.

Spinal cord injuries – the treatment of which costs in excess of $3 billion per year in the U.S. – often result in the impairment of locomotor, sensory and autonomic functions. Those individuals who suffer from acute spinal cord injuries experience serious functional deficits – including paraplegia and tetraplegia. This is caused by the degeneration of the spinal pathways that carry nerve signals from the brain to the extremities, which leads to the loss of both mobility and sensitivity to the areas below the site of the injury.

IL-37 Provides Hope

Researchers at the University of Barcelona (UAB) have identified a therapeutic target for people with severe spinal cord injuries based on their recent work with mice. The use of a protein called IL-37 that prevents the loss of myelin – the sheath that insulates the nerve fibers that allow signals to be transmitted from the brain to the rest of the body – has shown that it can increase mobility in mice following an injury.

Dr. Ruben Lopez Vales of UAB’s Department of Cell Biology, Physiology and Immunology, which is part of the school’s Institute of Neuroscience and the Centre for Networked Biomedical in Neurodegenerative Diseases (CIBERNED) coordinated the team of scientists to perform the study, which yielded some potentially encouraging results. The outcomes of the study were published in the online version of the Proceedings of the National Academy of Sciences (PNAS).

IL-37 has shown the ability to suppress inflammation following a spinal cord injury and minimize both the degeneration of spinal tissue and functional disabilities. IL-37 was initially identified more than 15 years ago, but its function has been difficult to prove as it’s not synthesized in mice. By using a genetically modified mouse with the ability to synthesize IL-37, researchers were able to prove that it increases mobility if administered immediately after an injury.


Limiting Myelin Loss

Lysophosphatidic acid, a lipid that acts as a signaling molecule between cells that make up an organism, plays a significant role in the degenerative processes associated with spinal cord injuries. Researchers have observed that increases in lysophosphatidic acid correlate with the loss of myelin. A biological receptor known as LPA1 has been identified as allowing the lipid to multiply the degenerative effects of spinal cord injuries.

In experiments using mice, the use of a drug that prevents the interaction between lysophosphatidic acid and LPA1 led to a marked reduction in myelin loss and improved locomotor performance following an injury. While some mice still displayed inconsistent or uncoordinated locomotion, 87 percent of the mice responded to the administration of the drug with what was deemed to be normal, coordinated locomotion.

In addition to its potential application in instances of severe spinal cord injuries, IL-37 also may prove useful in the treatment of neurodegenerative illnesses, as inflammation plays a role in these conditions as well. Clinical trials using anti-inflammatory drugs like methylprednisolone have proven ineffective, so IL-37 could bridge that gap in the near future.