Queen’s University Belfast has been awarded £425K by the Biotechnology and Biological Sciences Research Council (BBSRC) for its new study of Multiple Sclerosis (MS) treatment.
Currently some 100,000 people in the United Kingdom have MS which affects the ability of nerve cells in the brain, spinal cord and eye, to communicate with each other effectively.
The new study, based in Queen’s Centre for Infection and Immunity (Cii), will investigate how parts of the immune system can help repair the damage caused by MS attacks.
The project is being led by Dr Denise Fitzgerald, who herself experienced a condition similar to MS, called Transverse Myelitis when she was 21. As a result of inflammation in her spinal cord, she was paralysed in less than two hours.
Dr Fitzgerald had to learn to walk again as the damage in her spinal cord repaired itself over the following months and years. It is this natural repair process that often becomes inefficient in MS, a chronic life-long condition, and this failure of repair can lead to permanent disability.
Boosting this natural repair process in the brain and spinal cord is the next frontier in treating MS, as currently there are no drugs that are proven to do so.
Speaking about the importance of the new study, Dr Fitzgerald said: “The central goal of our research is to identify new strategies to treat MS and other inflammatory and demyelinating disorders.”
Nerve cells communicate by sending signals along nerve fibres which are contained within a fatty, insulating, protective substance, known as Myelin. In MS, Myelin is attacked and damaged (demyelination) which can lead to either faulty signalling by nerves, or death of the nerve cells. As a result, patients experience loss of nerve function in the area of the brain/spinal cord that has been damaged. This research project centres around understanding Myelination, a process of insulating the nerve fibres with Myelin, and Remyelination, a natural regenerative process that replaces damaged Myelin.
We already know that the immune system is implicated as a potential culprit in MS, as the damage is thought to be caused by inflammation in the central nervous system (CNS; brain, spinal cord and optic nerve). But in recent years we have learned a great deal about how the immune system also supports tissue repair in the CNS.
In particular, there is a group of immune cells called T cells which have recently been shown to support remyelination. There are different subsets of T cells, however, and little is still known about which subsets are beneficial in this process. In our study we aim to discover if these different T cell subsets influence remyelination of the CNS, and if ageing of the T cells impairs remyelination in older individuals.
The outcomes of this study will include new knowledge of how the immune system, and T cells in particular, influence remyelination in the Central Nervous System. We will also learn a great deal about how ageing affects the ability of T cells to help tissue repair.
Given the profound neurological impairments that can accompany ageing, and our growing aged population, is it imperative that we understand how normal CNS repair can become impaired with age.
“By understanding this process of CNS repair in detail, we will also gain an insight into other inflammatory and demyelinating disorders, ” Dr Fitzgerald added.
Queen’s Centre for Infection and Immunity (Cii) delivers high-quality research programmes to develop new treatments for infection and inflammatory diseases. Based in a newly built state of the art facility equipped with cutting edge technology, it has capacity for 200 researchers. Cii is leading international programmes investigating the role of innate and adaptive immune responses to infection and tissue injury and how these might be targeted to develop effective new treatments.
BBSRC invests in world-class bioscience research and training on behalf of the UK public. Our aim is to further scientific knowledge, to promote economic growth, wealth and job creation and to improve quality of life in the UK and beyond.