Simon Murray is a Lecturer and Laboratory Head in the Department of Anatomy and Neuroscience.
He graduated as a Physiotherapist in 1992, worked for several years before returning to study and graduating with his PhD in 2000. He spent 3 years as a post-doctoral fellow at the Skirball Institute at the New York School of Medicine, before returning to Australia to work at the Florey Neuroscience Institutes in the Multiple Sclerosis Research Division. He moved his laboratory to the Centre for Neuroscience in 2005, and joined the Department of Anatomy and Neuroscience in 2010. His research primarily focuses on myelin biology, in particular understanding the nature of the signals between neurons and glia that regulate normal myelination during development and myelin repair after nervous system injury. He has a particular interest in a family of growth factors known as the neurotrophins, and how neurotrophin-based strategies could be developed to promote myelin repair in the context of demyelinating disease such as multiple sclerosis.
Neurotrophin and Myelin Laboratory.
Demyelinating diseases of both the peripheral and central nervous system have a devastating human impact. There is currently an incomplete understanding of the factors that initiate, promote and maintain the interactions between neurons and glial cells that are vital for myelination. Our laboratory is interested in understanding the nature of signals that control myelination. Our focus centres on a family of growth factors known as the neurotrophins, and the influence they exert on both peripheral (PNS) and central nervous system (CNS) myelination. We use a variety of molecular, cellular, biochemical and genetic techniques to investigate these events.
We have recently identified that the neurotrophin 'brain derived neurotrophic factor' (BDNF) plays an important role in promoting both central and peripheral nervous system myelination. Our data indicate that BDNF activates distinct receptors that are expressed on neurons and glial cells to regulate myelination. We are currently adopting genetic approaches to investigate the precise roles played by these receptors to promote both the normal development of myelin and remyelination following a demyelinating insult.
We have also developed novel low molecular weight peptide mimetics of BDNF designed to selectively activate its receptors. We are interested in examining whether these mimetcs can (i) activate their respective receptors and initiate key intracellular signalling cascades in vitro
and (ii) promote myelin repair in vivo
using animal models of central and peripheral nervous system demyelination.