According to a study published online by the Journal of Neuroscience, researchers have gained new insight into how Schwann cells protect and repair damage caused by trauma and disease. These findings could lead to future treatments for the repair and improvement of damage to the peripheral nervous system.

Schwann cells insulate the nerve cells in the peripheral nervous system – all the nerves outside of the brain and spinal cord.

The study, funded by the Wellcome Trust, was conducted by researchers from the Peninsula College of Medicine and Dentistry, University of Exeter, in collaboration with researchers from Rutgers University, Newark and University College London.

Not only does the peripheral nervous system (PNS) control the functions of all the organs in the body, it also transmits motor information that allows us to move, and sensory information that allows use to feel the sun on our face.

The PNS can be damaged through trauma and can occur in patients with common inherited conditions, such as Charcot-Marie-Tooth (CMT) disease, and in diabetic neuropathy (suffered by almost half of those with diabetes).

Symptoms of PNS damage include problems with sexual function, bladder control, blood pressure regulation, digestion and loss of sensation in the hands and feet.

Schwann cells provide the myelin sheath (insulation) for the nerve cells that carry electrical signals to and form the spinal cord. The cells can revert back to an immature ‘repair’ cell due to their plasticity, therefore allowing them to repair damage to the PNS. Even though Schwann cells can repair damage effectively, incomplete repair, such as after the severance of a nerve, may result in pain and long-term loss of function.

As Schwann cells have the ability to demyelinate they can become susceptible to diseases, such as CMT. Approximately 1 in 2,500 individuals are affected by CMT. There are many different genes in CMT, and variations in these genes can result in cycles of repair and re-myelination (re-insulation) which can cause long-term damage and the death of both nerve and Schwann cells. Currently there is not treatment available for CMT and patients experience increased sensory and motor problems which could leave them permanently disabled.

These findings will lead to treatments that improve damage from severe trauma and break the cycle of damaged causes by CMT, say the researchers. In addition, the team believe that there may also be potential to improve repair in cases of diabetic neuropathy.

The researchers have found that cJun, a DNA binding protein, plays a vital role in the plasticity that allows a Schwann cell to revert back to the active repair state. This protein can be triggered by numerous different pathways that transmit signals from the surface of the Schwann cell to the nucleus. They found that the p38 Mitogen Activated Protein Kinase Pathway appears to play an important role: it is stimulated following PNS damage and may encourage the process of repair; conversely it may be abnormally activated in demyelinating diseases such as CMT.

Professor David Parkinson, Associate Professor in Neuroscience, Peninsula College of Medicine and Dentistry, University of Exeter, explained:

“The findings of our research are exciting because we have pinpointed and are understanding the mechanism by which our bodies can repair damage to the peripheral nervous system. With further investigation, this could well lead to therapies to repair nerve damage from trauma and mitigate the damage which relates to common illnesses, such as CMT.”

Written By Grace Rattue