Neuroimmunology and Remyelination Laboratory
We are multi-disciplinary group straddling the fields of immunology, genetics and myelin biology, with a particular interest in the intersection of these disciplines in MS susceptibility, severity and recovery.
Our team works collaboratively to investigate questions ranging from basic biology, such as the effect of receptor tyrosine kinases on myelination by oligodendrocytes, through to translational research, developing novel therapeutic treatments for MS.
We use a variety of techniques and mouse models of MS, as well as directly studying the human disease. We have a number of projects available that are suitable for both Honours and PhD students who would like the opportunity to explore the interface of genetics, immunology and neuroscience.
A glimpse at our researchThe TAM family and Multiple SclerosisMultiple Sclerosis Susceptibility Genes and the Immune SystemModulating innate immune cells as a potential therapy for Multiple SclerosisTyro3 in myelination and remyelinationFunctional Consequences of Multiple Sclerosis Risk Genes
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.
The primary target of attack in MS is the oligodendrocyte, and the myelin produced by these cells. The loss of myelin ensheathing 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.
The emphasis of our collective work is therefore to make fundamental discoveries concerning the molecular pathogenesis of progressive MS. From these studies we aim to identify and validate molecular targets to enable the development of diagnostic agents for detection of subclinical progression and of therapeutics to potentiate remyelination thereby inhibiting disability progression.