Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS), and is a common cause of neurological disability, affecting over 2 million people worldwide, including over 21,000 people in Australia. MS is the most common neurodegenerative disease of young adults in our community, unfortunately striking people who are otherwise in the prime of their life.
The primary target of attack in MS is the oligodendrocyte, and the insulating myelin produced by these cells. The loss of myelinated axons, a process known as demyelination, impairs nerve function by slowing and disrupting electrical impulses, as well as by exposing axons to further inflammatory attack. Following a demyelinating event some spontaneous remyelination occurs but it is often incomplete, and as the disease progresses remyelination fails, ultimately leading to the degeneration of exposed axons.
There is an emerging consensus that the progression of disability in MS correlates with the accumulation of axonal degeneration, which in turn is influenced by the extent of demyelination and the loss of oligodendrocytes. Current MS therapies, however, are anti-inflammatory, suppressing the immune response, and although efficient in limiting the relapses that characterise the early phase of MS, they do not prevent patients from entering the secondary progressive phase of the disease, for which no treatments are available.
We aim to make fundamental discoveries that will improve our capacity to treat and ultimately prevent this debilitating disease.