Category Archives: Our Fellows Profile

Professor Sylvia Gustin (PhD, BPsych, MPsych) is Founding Director of the NeuroRecovery Research Hub at the University of New South Wales and Director of the Centre for Pain IMPACT (*investigating pain mechanisms to advance clinical translation) at Neuroscience Research Australia. She received her PhD in Neuroscience from the University of Tubingen, Germany, in 2006. Prof Gustin has been using multimodal neuroimaging techniques to investigate the central circuits underlying chronic pain, spinal cord injury neuropathic pain and rehabilitation. Her program of research forms a translational pipeline where her basic science research informs the development of novel therapeutic interventions that are translated to improve the lives of people with a disorder affecting the brain and spine. She develops and tests new technology treatments (e.g., Virtual Reality Walking and gamified Brain-Computer Interface Neuromodulation) to ameliorate chronic pain, for example neuropathic pain after spinal cord injury, phantom pain after amputation or orofacial pain. Her research also focuses on developing and testing novel haptic virtual reality walking treatments/interfaces to offer restoration of somatosensory perception among individuals previously classified as having total sensorimotor loss. Her research is funded by the Rebecca L. Cooper Medical Research Foundation, the Australian National Health and Medical Research Council (NHMRC), the Medical Research Future Fund (MRFF), International Association for the Study of Pain (IASP), US Department of Defence (DoD), NSW Defence Innovation Network and NSW Health.

Research

THE AVATAR PROGRAM: SPINAL CORD INJURY AND RELATED DISORDERS: DISCOVERY TO CURE
Around 350 Australians are affected by a spinal cord injury (SCI) each year, many of them at a young age. The effects of a spinal cord injury are major: they can impair many critical functions that are easily taken for granted. Movement, sensation, blood pressure control as well as bowel, bladder and sexual function can all be affected. Complete spinal cord injury (SCI) is associated with total loss of sensorimotor function below the level of injury. However, in a 2018 breakthrough finding A/Prof Gustin revealed that half of all people suffering from a complete SCI still have surviving spinal somatosensory nerve fibres. This finding has received significant attention from the global science and SCI community because it reflects a paradigmatic shift in science and culture – for the first time, individuals who thought they could not move or feel below the site of injury have the potential to feel again. However, currently, there are no effective pharmacological/biological interventions to promote or restore touch perception after SCI. Consequently, there is an urgent need to develop new therapies to promote/restore touch perception after complete SCI.

Although loss of mobility is often considered the most serious consequence of SCI, people with SCI consistently rate pain as one of the most difficult problems to deal with. SCI neuropathic pain is experienced below the zone of injury and is described as sharp, burning, unbearable and terrifying. Critically, SCI neuropathic pain remains minimally responsive to existing pharmacologic and non-pharmacologic treatment. Although pharmacological agents (e.g., opioids and antiepileptics) are treatment mainstays, most provide only a third of patients 30% pain reduction and are associated with numerous negative side effects, e.g. toxicity, addiction and abuse. Consequently there is an urgent need to develop new SCI pain therapies.

The Avatar Program will address these urgent needs by developing and evaluating interventions that can provide touch restoration and pain amelioration via the primary source of touch and pain: the human brain. Over the last 13 years A/Prof Gustin has undertaken fundamental research to unravel the critical neurochemical, structural and functional brain changes that underlie SCI Rehabilitation and SCI neuropathic pain. Firstly, she has identified thalamic ‘biomarkers’ of spinal cord injury neuropathic pain and delivered the thalamocortical model for the development and chronification of neuropathic pain following SCI. Secondly, she has provided the first objective evidence that 50% of people with a complete SCI still have intact nerve fibres which can likely still influence perception and performance. In her AVATAR program, Prof Gustin aims to translate the gained knowledge of her fundamental research into treatment.

Prof Gustin has developed two new approaches that target the neurochemical and functional thalamic alterations which her research previously revealed to ultimately treat SCI neuropathic pain. (1) Gamified Brain-Computer Interface Neuromodulation (gBCI-N) intervention teaches individuals to gain control over their brain activity via EEG biofeedback in a way that reduces their pain. (2) Virtual reality walking (VRWalk) therapy targets cortical and sub-cortical disruption associated with SCI neuropathic pain by reinstating sensorimotor input using visual illusion and thereby reducing pain. (3) Lastly, drawing on her recent discovery and innovations in virtual reality (VR) embodiment technology, she will develop an entirely novel intervention to restore touch perception among individuals previously classified as having complete perceptual loss. Virtual Reality Haptic Walking (VRHapticWalk) intervention simultaneously enhances surviving somatosensory spinal nerve fibres and somatosensory (touch) signals in the brain in an effort to restore touch perception among people previously classified as having complete perceptual loss.

If you want to know more about Prof Gustin’s research, please visit her website: www.neurorecoveryresearch.com

Dr Joshua Ooi is a Senior Research Fellow at the Centre for Inflammatory Diseases, School of Clinical Sciences, Monash University. His research focusses on understanding why the immune system sometimes targets self-proteins and causes autoimmune disease. He has identified the precise autoimmune targets in a rheumatic autoimmune disease known as ANCA-associated vasculitis and will use this Fellowship to translate that knowledge into new targeted therapeutics.

Research

ANCA-associated vasculitis is a severe autoimmune disease that causes the destruction of the kidneys and lungs. It has a high morbidity and high mortality rate, 40% in 5 years. Furthermore, current treatments for this disease are a combination of steroids and global immunosuppressants that wipe out most of the immune system leaving patients vulnerable to life-threatening infections. In recent years, Dr. Ooi has made significant breakthroughs in understanding the cause of disease as well as the specific parts of the kidneys and lungs that are “attacked” by the immune system. His work has been published in the top nephrology journal, Journal of the American Society of Nephrology, as well as in other prestigious medical and science journals including, Proceedings of the National Academy of Sciences, The Journal of Clinical Investigation and Nature.

Armed with this new knowledge, the overall aim of Dr. Ooi’s project is to increase the effectiveness of treatment by developing new therapies that shut down the part of the immune system that is attacking self-proteins, while leaving protective immunity against invading pathogens intact. One of Dr. Ooi’s recent discoveries, published in Nature, details how specific immune cells, known as regulatory T cells, that recognise proteins found in the kidneys and lungs can confer protection from autoimmune disease. Based on this finding, Dr. Ooi has developed new experimental therapies that can induce this protective cell type in patients. Dr. Ooi will use this Fellowship to translate his experimental findings into a clinical treatment.

Dr Ooi’s work has continued to receive prestigious awards including the Australian Tall Poppy Science Award by the Australian Institute of Policy and Science, the Senior Gordon Ada Award from the Australia and New Zealand Society of Immunology and the Next Step Initiative Award from the Department of Innovation, Industry and Science.

Professor Bingyang Shi is the chair of nanomedicine and a biomedical engineer at the University of Technology Sydney, Faculty of Engineering and IT. He is a global leader in nanomedicine for brain disease therapy.

Professor Shi’s research ambition is to overcome the difficulty of traversing the blood–brain barrier, successfully delivering therapeutic agents to treat cancers and other brain disease. The blood–brain barrier acts as a cellular barrier that prevents toxins, foreign materials and other dangerous molecules from entering the brain, however as a consequence this poses major challenges for getting therapeutic molecules into the brain. To overcome this, Professor Shi has developed several core patented technologies for brain delivery systems (e.g., Bio-NPs and Glu-NPs), set up collaboration networks across multiple countries, and fostered close connections with industry and hospital partners to drive the delivery of a bench-to-bedside pipeline to improve outcomes for individuals living with brain cancer.

Professor Shi’s research has delivered more than 100 scientific papers as a senior author in well-known journals including Nature Nanotechnology, Science Translational Medicine, Science Advances, and Nature Communications. His work has been cited more than 11,000 times worldwide. He has also invented several patented drug delivery technologies designed to carry gene therapies and other medicines across the blood brain barrier, leading to IIT (phrase 0) clinical trials.

Professor Shi founded and is the executive editor-in-chief of Exploration, a Wiley interdisciplinary journal with an Impact factor of 22.5. The journal explores new insights and methods at the nanoscale, inspiring multidisciplinary collaborations to address challenges in life sciences, medical sciences and physical sciences.

Research

More than 1,000 Australians are diagnosed with brain cancer each year, yet survival rates and quality of life have remained largely unchanged for decades. Current treatments are limited by the blood–brain barrier, high genetic variability between patients and a lack of therapies tailored to individual tumour biology.

The Fellowship program aims to deliver an Australia first personalised therapy platform for brain cancer, designed to maximise survival and quality of life.

Building on Professor Shi’s patented brain drug-delivery technologies, AI-driven target discovery tools and proven precision therapy strategies, he will establish a long-term, multidisciplinary translational research pipeline that integrates discovery, engineering and patient-responsive testing.

Professor Shi’s Rebecca Cooper Fellowship research will:

• identify patient-specific therapeutic targets using AI-enabled profiling of Australian brain cancer samples
• engineer scalable, clinic ready nanotherapeutics capable of crossing the blood–brain barrier
• validate treatments using next generation brain tumour-on-chip models that reflect patient-specific tumour biology and drug response.

This integrated approach will deliver a program of research that directly addresses the stagnant treatment pathway that has constrained progress in brain cancer therapy, while remaining adaptable to and capable of pioneering precision treatments for other debilitating neurological diseases.

Professor Eynon is Group Leader at the Australian Regenerative Medicine Institute (ARMI), Monash University, Australia. He earned his PhD degree with high distinction in 2010 from Porto University, Portugal. His areas of expertise are epigenetics, healthy ageing and exercise, an area for which he won the Young Tall Poppy 2021 & the 2024 Australian Epigenetics Alliance Excellence in Research awards. His expertise has been recognised by being selected to the ARC College of Experts in 2023. He is a former NHMRC Investigator Fellow (2021-2025), NHMRC Career Development Fellow (2018-2021), and ARC DECRA Fellow (2014-2016). He was recently awarded Hevolution/Am Fed Aging Research New Investigator Fellowship in Aging Biology. He published 125 papers in high-impact journals and focuses on the discovery of sex-specific molecular markers associated with exercise & healthy ageing. The Eynon lab uses a combination of wet-lab and bioinformatics analyses, with a particular focus on ‘omics’ datasets including DNA methylation, transcription factors, transcriptomics and proteomics.

Research

The UN declared 2021–2030 the “Decade of Healthy Ageing”, underscoring an urgent global need to extend healthy lifespan. In Australia, ageing is the main driver of chronic disease and escalating healthcare costs. Yet, we lack precise molecular tools to measure or modulate biological ageing in the tissues most critical for independence, such as skeletal muscle, cardiac muscle, and blood. Without these, we cannot effectively monitor ageing trajectories, personalise interventions, or evaluate emerging therapeutics.

My program will address this gap by delivering the world’s first multi-tissue, cell-type specific atlas of ageing biomarkers, with a focus on sex-specific differences. We will leverage a unique resource of ~90,000 human samples (males and females) from 322 cohorts across 17 tissues, and utilise advanced bioinformatics, multi-omics, and gene editing techniques to identify biomarkers that drive ageing. This will distinguish adaptive from harmful changes and enable precision exercise prescriptions, targeted therapeutics, and health policies informed by biological rather than chronological age.
By enabling early detection of biological ageing changes, these biomarkers will facilitate timely clinical interventions to preserve muscle function, prevent frailty, and reduce hospitalisation risk. This directly supports healthier ageing populations, reduces healthcare burdens, and significantly improves quality of life; core goals aligned with the Rebecca Cooper Foundation’s mission.

Associate Professor Katie Ayers is the Deputy Theme Director for Genomic Medicine and Co-Group Leader of the Reproductive Development Group at the Murdoch Children’s Research Institute (MCRI) in Melbourne. A/Prof Ayers completed her undergraduate studies in Genetics at the University of Otago, New Zealand, before obtaining her PhD from the Université de Nice Sophia Antipolis in France, supported by an EU/Marie Curie Scholarship. Research in A/Prof Ayers’ group focuses on understanding the genetic and molecular mechanisms underlying reproductive organ development and Variations/Differences of Sex Development (DSD). Specifically, she uses advanced genetic and functional genomics technologies to improve diagnostic rates and patient health and wellbeing. This includes pioneering the use of stem cell models of reproductive organs to study DSD. A/Prof Ayers has received several accolades, including the Alan Wilton Award from the Genetics Society of AustralAsia (2014) and the KY Cha Award in Stem Cell Technologies from the American Society of Reproductive Medicine (2025). She serves on the editorial boards of Sex Development and Biology of Reproduction, is Treasurer of the Australasian Society for Stem Cell Research, and sits on several international steering committees, including for the Vertebrate Sex Determination and SOX Transcription Factor meetings.

Research

A/Prof Ayers’ research focuses on understanding how human reproductive organs develop and why this can vary in some people including those born with a Difference of Sex Development (DSD). Indeed, more than one baby in every 100 is born with a DSD. This means their sex chromosomes, hormones, or reproductive organs do not develop in a typical way. These differences can affect physical development, fertility, hormone health, and long-term wellbeing. Some people with DSD may face a higher risk of developing gonadal cancer, creating difficult decisions about monitoring, treatment, and surgery for children and families.

For people born with a DSD, finding the genetic cause can help doctors choose the best care, support families, and improve health outcomes. A/Prof Ayers and her team have already more than tripled the number of people who receive a genetic diagnosis by developing specialised genetic tests and discovering new genetic causes of DSD. However, for many DSDs, fewer than half of individuals currently receive a clear genetic answer. This is partly because scientists do not yet fully understand all the genes and DNA regions needed for reproductive organ development, and because there are limited laboratory tools to test new discoveries.

Supported by this Rebecca L. Cooper Foundation Fellowship, A/Prof Ayers and her group will work to identify new genetic causes of DSD and better understand gonadal cancer risk. They will investigate DNA changes in patients that lie outside of the genes. They will create cutting-edge laboratory models of developing human reproductive organs using stem cells and use these to test genetic findings and study how gonadal cancers arise. This research aims to give more individuals and families clear answers, improve cancer risk prediction, and support more personalised and informed care for people with DSD.

Professor Susanna Park PhD leads a multidisciplinary research program investigating assessment strategies, treatments and risk factors in neuropathy and neuromuscular disease at the University of Sydney. She was awarded her PhD from the University of New South Wales and undertook postdoctoral training at the Institute of Neurology, University College London. She has shown outstanding team leadership in research, securing significant research funding, publishing >150 publications and managing a collaborative research team. Her work has enabled real-time monitoring of axonal degeneration in neurotoxic chemotherapy-treated patients, via novel neurophysiological assessment tools, which have been adopted into research programs across 6 countries in chemotherapy neuropathy clinical research and clinical trials. Park has received significant awards, including the 2018 AW Campbell award from the Australasian Neuroscience Society for best contribution to neuroscience in the first 5 postdoctoral years and a NHMRC Career Development Fellowship (completed 2023). Park’s international leadership standing is demonstrated by leadership positions in international multidisciplinary research consortia groups, including the Peripheral Nerve Society Toxic Neuropathy Consortium.

Research

More people are living for longer following cancer treatment. However, treatment toxicities such as chemotherapy-induced nerve damage threaten cancer survival, leading to early chemotherapy discontinuation and chronic loss of sensation, pain and disability. Nerve damage is a major side effect of cancer treatment, affecting up to 40% of cancer survivors treated with common therapies.

To address this growing challenge, Prof Park leads a translational neurology program focused on the biological mechanisms of axonal degeneration, the process central to chemotherapy-induced nerve damage and many other neurodegenerative diseases.

Over the next five years, Prof Park and her team will develop metabolic, genetic and protein signatures of axonal degeneration from blood samples to develop clinically relevant biomarkers. These biomarkers will enable earlier diagnosis and targeted therapeutic interventions for patients with chemotherapy-induced nerve damage and other neurodegenerative conditions, ultimately transforming both diagnostic practices and treatment strategies worldwide.

Associate Professor Joanne Reed is Director of the Centre for Immunology and Allergy Research at Westmead Institute for Medical Research and an Adjunct Associate Professor at the University of Sydney. She received her PhD in Immunology from Flinders University, South Australia in 2009 and was awarded an NHMRC CJ Martin Fellowship for postdoctoral training at New York University (2010-2013) and Australian National University (2013-2014). Reed relocated to the Garvan Institute in 2015 where she rose to the position of Group Leader of the Rheumatology and Autoimmunity Lab and Conjoint Senior Lecturer at UNSW. In 2021 she was recruited to the Westmead Institute and University of Sydney where she established the Autoimmunity and Amyloidosis Lab.

Reed leads a translational research program focused on using genomic technology to understand the causes and progression of autoimmune and amyloid diseases to inform precision medicine approaches. She currently serves as a Council Member for the International Union of Immunological Societies (IUIS) and Australian and New Zealand Society for Immunology (ASI) and is co-chair of the ASI Advanced Immunology School.

Research

Autoimmune disease occurs when the immune system’s cells that normally attack invading viruses and bacteria go “rogue” and attack healthy parts of the body. In rheumatic autoimmune disorders such as Sjogren’s disease and systemic lupus erythematosus, rogue immune cells frequently damage connective tissues (joints, bone, muscles, and skin) and a diverse array of other major organs (heart, kidneys, blood, brain). There is no cure and treatments are limited to drugs that indiscriminately suppress the immune system, causing side effects and vulnerability to infection. The goal of our research is to understand where rogue cells originate and how they differ to normal immune cells so that we can selectively target and eliminate these disease-causing cells.

Previously our team identified rogue immune cells responsible for damaging the skin and kidneys in patients with Sjogren’s disease. We identified genetic features of rogue cells that were distinct to normal immune cells and could be targeted by therapies. However, the technology to identify rogue immune cells is expensive, time consuming and requires highly specialised expertise, making it challenging to screen large numbers of patients. With the support of the Rebecca Cooper Fellowship, the team will study rogue immune cells in patients with rheumatic autoimmune diseases and humanised mouse models to:
1) Develop a simplified and low-cost test that could be applied in the clinical diagnostic laboratory to identify drug targets on rogue cells; and
2) Uncover the origins of rogue cells and test new treatments in a mouse model of disease.
The establishment of innovative technology to detect rogue immune cells and pre-clinical models to validate treatments to eliminate rogue cells has the potential to personalise clinical care for patients with autoimmune disease.

Michael Lazarou is an Associate Professor of Medical Biology at WEHI with a co-appointment at Monash Biomedicine Discovery Institute. He completed his PhD studying mitochondrial disease in 2008 at La Trobe University. His post-doctoral studies were conducted at the National Institutes of Health (USA) where his research focused on PINK1 and Parkin and their role in maintaining mitochondrial health via mitophagy (a pathway that degrades damaged mitochondria), which led to his receiving the 2013 ASBMB Boomerang Award. A/Prof Lazarou’s discoveries have formed the basis of modern models of PINK1/Parkin mitophagy and general autophagy. He uses advanced imaging technologies assisted by AI approaches developed by his team, and combines gene editing of human cell lines, including stem cell derived neurons, with cell biology and biochemical approaches to understand the mechanisms of mitophagy. His autophagy and mitophagy discoveries have been recognised as major breakthroughs by Science Signaling, Journal of Cell Biology, and Autophagy. A/Prof Lazarou has received multiple awards including holding an Australian Research Council Future Fellowship (2017–20), and the 2022 ASBMB Shimadzu Research Medal. A/Prof Lazarou currently serves on the editorial board of Journal of Cell Biology, and is co-founder and scientific advisory board member of Automera, a company focused on harnessing autophagy driven degradation to treat disease.

Research

Mitochondrial dysfunction has been identified as a key player in the development of Parkinson’s disease, and this highlights the need to develop therapeutic approaches that target mitochondrial health. A/Prof Lazarou aims to translate fundamental research into mitophagy towards discovering a drug therapy that will have significant benefit in improving mitochondrial health in Parkinson’s disease. This research has the potential to improve treatment options and improve quality of life for people living with Parkinson’s disease which currently has no drug to slow or stop disease progress. The Foundation’s support will allow A/Prof Lazarou to advance his discovery research toward developing therapeutics that target mitochondrial dysfunction that can have impact in Parkinson’s disease and beyond, including other forms of neurodegeneration with mitochondrial involvement (e.g. Alzheimer’s).

Associate Professor Catherine Satzke leads the Translational Microbiology Group at the Murdoch Children’s Research Institute (MCRI), overseeing a comprehensive, high-quality microbiological research program, partnering with clinicians to deliver translational outcomes.

A/Prof Satzke’s research is focused on major global bacterial pathogens including Streptococcus pneumoniae (the pneumococcus) and Streptococcus pyogenes (group A streptococcus, GAS). She has created powerful new knowledge leading to major changes in tools for pneumococcal studies globally. A/Prof Satzke led the update of World Health Organization (WHO) standards for pneumococcal carriage studies enabling investigators to conduct high quality and consistent carriage studies in more than 70 countries for pneumococcus and other bacterial species. A/Prof Satzke’s research has provided evidence of vaccine success in Fiji, Laos and Mongolia, leading to continuation of national pneumococcal conjugate vaccine (PCV) programs, improving protection against diseases including pneumonia and meningitis.

A/Prof Satzke received the prestigious international Robert Austrian Research award (2012), the Frank Fenner award (top national mid-career award) in 2017 and was appointed as a Fellow of the Australian Society for Microbiology (ASM) in 2019. Catherine was an inaugural veski Inspiring Women Fellow (2016-2018, $150K) and held a NHMRC Career Development Fellowship (2015-2020).

Research

The lung disease pneumonia is the leading killer of children worldwide, with >100 million cases and 800,000 deaths annually. Pneumonia from bacterial-viral coinfection is more deadly than from either pathogen alone.

Streptococcus pyogenes (group A streptococcus, GAS) is a major cause of respiratory disease globally. Coinfection with influenza virus increases the frequency and severity of GAS disease. This increase was illustrated in the recent surge in GAS lung disease globally, with many of these cases also being infected with influenza. Despite this recent surge in cases, little is known about the mechanisms which drive influenza-GAS lung disease.

Catherine and her team have established new models to gain important insights into lung disease. With support from the Rebecca Cooper Foundation, Catherine and her team will take clinical isolates from globally circulating strains of GAS and test these using their models to determine the following:

1)The mechanism of host damage in influenza-GAS coinfection.
2)The mechanism by which influenza increases GAS lung disease.
3)The importance of other respiratory viruses for GAS lung disease.

This program will provide critical information for future treatment and prevention strategies for infectious lung disease worldwide.

Prof. Ethan Goddard-Borger is a Laboratory Head within the Chemical Biology Division at The Walter and Eliza Hall Institute of Medical Research (WEHI). He received his PhD with Distinction as a Hackett Scholar in 2008 from the University of Western Australia. From 2009-2013, he was a Canadian Institutes of Health Research Postdoctoral Fellow at the University of British Columbia, where he developed preclinical drug candidates for lysosomal storage disorders. In 2013, Ethan returned to Australia as a VESKI Innovation Fellow to establish his independent research program at WEHI in Melbourne. His laboratory is developing new therapeutic approaches to treating inflammatory diseases of the respiratory tract, including asthma, COPD, IPF and CF. Ethan was awarded the 2022 Burnet Prize and 2024 AGS Shimadzu MCR award for his work.

Research

Chronic respiratory diseases, such as asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), are a major source of morbidity and mortality worldwide. The 2018 Australian Bureau of Statistics National Health Survey revealed that 11% of Australians have asthma. Meanwhile, the World Health Organization (WHO) reports that COPD is the third leading cause of death worldwide (3.23 million in 2019), and the fifth leading cause of death in Australia.

A common feature of these diseases is the over-production of a viscous mucus that patients struggle to clear from their airways. This mucus accumulates over time and forms obstructions in the airways, impairing lung function and increasing the likelihood of infections developing. There is a substantial unmet need for effective mucus-thinning (mucolytic) drugs to better manage this problem. An efficacious mucolytic drug would provide substantial benefits to many suffering from these debilitating, incurable diseases.

My research tackles this problem by first building a thorough understanding of the molecular mechanisms governing pulmonary mucus rheology. My team are applying cutting-edge proteomic and biochemical technologies to understand how interactions between proteins in the mucus can drive changes in the bulk physical properties of the mucus in the lungs. With this knowledge, my laboratory will set about developing new tests to help identify those patients who are most at risk of developing airway obstructions. We will also identify and validate new targets for the development of mucolytic drug candidates. This work will deliver valuable data sets, biomarkers and potentially even early drug candidates that will contribute to a better understanding and improved management of chronic respiratory diseases.