Yona Goldshmit


  • yona.goldshmit@monash.edu


1997-1999 Physiotherapist in Loewenstein Hospital Rehabilitation Centre in Israel working with head trauma and spinal cord injury patients.
2000-2001 Completed the degree of Master in Neurobiochemistry at the Tel-Aviv University, Israel, with summa cum laude. This research led to a publication in 2001 in the Journal of Biological Chemistry.

2001-2004 PhD at the Centre for Neuroscience, University of Melbourne. The project involved examination of the regulation of neurite outgrowth/axonal regeneration following spinal cord injury and was centred on the role of the receptor tyrosine kinase, EphA4. This work was published in the high impact journal, Journal of Neuroscience (2004) (YG5; Impact factor 7.51; Times cited 44), and also led to a patent application (Patent application “A method of treatment and agent useful for same” by the University of Melbourne and University of Queensland; application No. 2005001363 filed at Australian Patent Office on 8 Sept 2005, for blocking EphA4 after brain injury and disease. At the moment it is in the process of negotiations with pharmaceutical company for commercialising this work.).

2005-2007 Awarded a SpinalCure Australia Fellowship and was able to continue assessing this therapeutic potential by blocking EphA4 to improve neuronal regeneration after spinal cord injury. The promising results of this study led thegroup to apply for and receive a grant from the Victoria Neurotrauma Initiative (VNI) in 2006, in order to design small peptide molecules that block the interaction between EphA4 and ephrins.

2008-2011 Awarded a prestigious VNI Early Career Research Fellowship in the Australian Regenerative Medicine Institute at Monash University to determine the role of EphA receptors in non-human primate brain development and after injury.

Research interests

The research aims are to develop a strategy to limit neuronal death and degeneration following traumatic brain and spinal cord injury.

This project will focus on ephrins and their Eph receptors, which are molecules that are expressed in the brain and guide the formation of neuronal pathways during development. The Eph and ephrin molecules are upregulated after trauma in the brain and spinal cord at the site of the injury, and shown to be inhibitory for neuronal regeneration and mediating the glial scar formation after brain trauma in rodent and primate models.

However, in the zebrafish model axons do regenerate after spinal cord injury.

In order to understand the mechanism involved in glial scar formation and neuronal degeneration after trauma, I will examine the zebrafish model, focusing on the role of EphA receptors in glial scar formation.