In multiple sclerosis (MS) there is specific destruction by the immune system of the protective myelin sheath that coats nerve fibres. However, there is also evidence that there may be an initial disruption to the nerve fibres before myelin damage occurs. The molecules which may contribute to, or initiate, such damage in MS are becoming known. By targeting these molecules it may be possible to limit the destruction which occurs to nerve fibres in the brain and spinal cord and so promote a better clinical outcome for people with MS.
Mr Taghian will be working in with an established research group at Monash University that has focussed on understanding the mechanisms of degeneration and regeneration in the nervous system in conditions such as stroke, MS and Alzheimer’s disease.
The group has recently shown that signalling through a pathway involving a molecule known as Nogo, may govern the earliest stages of nerve fibre damage in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). They have shown that blocking this pathway can limit the extent of nerve damage. They also have preliminary data identifying some of the other molecules involved.
Mr Taghian will now more clearly define the roles played by these molecules and attempt to block the molecules which promote nerve fibre degeneration using novel strategies to deliver potential therapeutic agents to the brain and spinal cord.
This study will enable future research directed to the development of more specific therapeutic strategies to limit damage and promote repair in the chronically injured MS brain.
Updated: 30 June 2013
Updated: 04 January, 2012