Oligodendrocytes are the cells in the human brain and spinal cord (central nervous system) that produce the myelin sheath around nerves. Schwann cells do the same job in the rest of the nervous system (peripheral nervous system). These cells myelinate nerve fibres by extending processes which encircle the nerves many times to form a multi-layered sheath. Each nerve fibre has many myelin segments and in humans each segment can be over a millimeter in length, with gaps between the segments of about a thousandth of a millimeter. Myelin promotes rapid communication not only between different groups of nerve cells within the central nervous system, but also between nerve cells and muscles. This is because

wrapping myelin around nerves causes specialized pores at the nerve surface called sodium channels to become concentrated in the gaps between successive myelin wraps. These gaps are called nodes of Ranvier and their high concentration of sodium channels is crucial for the rapid electrical conduction of nerve impulses.

When myelin is destroyed, as in multiple sclerosis (MS) in the central nervous system, or Charcot-Marie-Tooth (CMT) disease in the peripheral nervous system, we lose functions for two reasons. First, the speed of nerve conduction slows because sodium channels diffuse away from the node, and secondly, without a myelin sheath the nerves start to degenerate. It is believed that nerve degeneration is linked to the disruption of the nodal sodium channels, and their dispersion is also believed to be at the root of other distressing aspects of these diseases such as pain. Demyelinating diseases are relatively common: there are about 80,000 people in the UK with MS and about 30,000 with CMT. Thus far there are no cures and no therapy halts disease progression.

There has been considerable progress in identifying the accessory proteins that persuade sodium channels to go to the node and remain there, primarily by knocking the genes that encode the proteins out in mice. This is how we discovered a group proteins that are encoded by a gene called Neurofascin which have a key role in "clustering" sodium channels. However, we have no idea how they do it. Therefore, two key question need to be answered. The first is, how does myelination cause Neurofascin proteins to assist in concentrating sodium channels at nodes of Ranvier? Secondly, why does loss of myelin cause sodium channels to disperse?