This is a confocal micrograph taken from the lesion core after a spinal cord injury. Nuclear EdU (red) shows the presence of newly differentiated cells which produce Schwann cell myelin (P0, green). These peripheral-like Schwann cells remyelinate central axons in the injured spinal cord and are important for spontaneous repair and functional recovery after spinal cord injury. Credit: King’s College London
Researchers have identified a molecular signal, known as ‘neuregulin-1’, which drives and enables the spinal cord’s natural capacity for repair after injury. The findings could one day lead to new treatments which enhance this spontaneous repair mechanism by manipulating the neuregulin-1 signal.
Every year >130,000 people suffer traumatic spinal cord injury and related healthcare costs are among the highest of any medical condition – yet there is still no cure or adequate treatment. Spinal cord injury has devastating consequences for muscle and limb function, but the central nervous system does possess some limited capacity to repair itself naturally.
For the first time researchers from King’s and Oxford have identified neuregulin-1, which signals from the surface of damaged nerve fibres during a process called ‘spontaneous remyelination.’ It is a period of natural regeneration that happens in the weeks following a spinal cord injury. The process takes place as a result of damage to spinal nerve fibres which have lost their insulating ‘myelin sheath’ However, this natural capacity for repair is not sufficient for full recovery and may account for the compromised function of surviving nerve fibres, which can affect balance, coordination and movement.
The researchers found that, in mice lacking the neuregulin-1 gene, spontaneous myelin repair was completely prevented and spinal nerve fibres remained demyelinated (i.e. unable to send nerve signals along the spinal cord).
Not only did neuregulin-1 drive spontaneous remyelination, but it also served as a molecular switch for cells within the spinal cord to transform themselves into cells with remyelinating capacity. This is unusual, according to the researchers, because the ‘Schwann’ cells with new remyelinating capacity normally only myelinate nerve fibres in the peripheral nervous system – not the central nervous system, as observed here.
Professor Bradbury said: ‘By enhancing this spontaneous response, we may be able to significantly improve spinal cord function after injury. Our research also has wider implications for other disorders of the central nervous system which share this demyelinating pathology, such as multiple sclerosis.’
http://www.kcl.ac.uk/ioppn/news/records/2016/March/Scientists-pinpoint-molecular-signal-that-drives-and-enables-spinal-cord-repair.aspx
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