Genetics study shows how cells adapt to help repair nerve damage
September 2017: Research uncovering the genetic mechanisms behind nerve damage and repair has been highlighted in the journal ‘Cell reports’.
Research led by the Director of the University of Edinburgh’s Centre for Genomic and Experimental Medicine, Professor Tim Aitman, has been chosen as a highlight in the most recent issue of the journal Cell Reports (Cell Reports 20, 2719–2734).
In the UK, 1 in 10 people over the age of 55 suffer from numbness, pain or muscle weakness in the body’s extremities. These are symptoms of peripheral neuropathies that arise following injury to nerve cells in the peripheral nervous system – the network of nerves outside the brain and spinal cord.
Undamaged nerve cells in the peripheral nervous system are supported and protected by Schwann cells. If a nerve cell is damaged, some Schwann cells undergo changes that allow them to prioritise nerve repair to fix the injury before it causes irreversible damage to the nerve. This study sheds light on the molecular and genetic processes that orchestrate these changes. Findings from this study could be used to identify drug targets to treat conditions that arise due to nerve damage.
The researchers also found that the molecular signals that cause Schwann cells to assume the role of repair cells are remarkably similar to the signals observed in the formation of some tumours. This suggests that on a molecular level, tissue repair is closely related to tumour formation, which can also improve our current understanding of cancer.
Our findings give us insight into how cells in the body adapts to injury. This knowledge will help identify drug targets for much-needed therapies to help patients with peripheral neuropathy and traumatic nerve injuries.
The study was carried out in collaboration with researchers from the University of Cambridge, University College London, and Imperial College London, and funded by the Medical Research Council and the Wellcome Trust.
Journal article (Cell Reports 20, 2719–2734)