MND Australia

MND Australia grants commencing 2025

MND Australia has awarded over $2.55 million towards motor neurone disease research projects commencing in 2025.

The grants awarded include the Bill Gole MND Research Fellowship, the MND Australia Postdoctoral Fellowship, the Scott Sullivan MND Postdoctoral Fellowship and 15 Innovator Grants (details of the research projects and recipients are available below).

This year, we are fortunate to have volunteers from our Lived Experience Network reviewing and providing feedback on lay project summaries. These are currently out for review and may be updated on the basis of that feedback. 

Research Fellowships

Image of Dr Azin Amin | University of Melbourne
Dr Azin Amin | University of Melbourne

Bill Gole MND Research Fellowship

In MND, one key reason motor neurons die is the accumulation of toxic protein clumps inside them. Normally, the body clears away this harmful “trash” through a natural process called autophagy, but in MND, this process becomes impaired. My project focuses on developing an innovative therapy using tiny proteins called peptides, designed to enter the brain, target motor neurons, and restore autophagy. These peptides have already shown promise in MND mouse models by enhancing autophagy and extending survival. By refining these peptides and testing them in various MND models, we aim to protect motor neurons and slow or even halt disease progression. This research could lead to new treatments that improve the quality of life for people living with MND.

Image of Dr Nathan Pavey | University Of Sydney
Dr Nathan Pavey | University Of Sydney

MND Australia Postdoctoral Fellowship

Recent advances in transcranial magnetic stimulation (TMS) technology, a non-invasive method of assessing brain function, have enabled the assessment of new excitability properties in motor neuron disease (MND). Cortical dysfunction occurs early in the development of MND and heralds a faster rate of disease progression, greater functional disability and more prominent weakness. The research encompassed by this MND Australia Postdoctoral Fellowship will assess new measures of cortical excitability dysfunction in MND patients to further our understanding cause of the disease.

Image of Dr Sophia Luikinga | University of Queensland
Dr Sophia Luikinga | University of Queensland

Scott Sullivan MND Research Fellowship

People living with motor neurone disease (plwMND) are known to have alterations in their body fat composition and metabolism. Fat molecules (also called lipids) are essential for the maintenance of motor neurons and muscles. Recently, I discovered that a subset of these lipids is unique to MND. However, this data is preliminary, and further tests will be necessary to assess if this is the case in a greater cohort of plwMND. We will assess the normal and abnormal ranges of the lipids that can then be communicated with specialists to be a biomarker for disease. Furthermore, we will assess the lipid biomarkers in a population of asymptomatic gene carriers to assess if these lipids are abnormal before symptom onset. Once this research is complete, I hope that this can help clinicians assess if drugs have a desired effect and how disease is progressing. This will in turn help with drug development and treatment strategies in the future.

Innovator Grants

Image of A/Prof Dominic Ng | University of Queensland
A/Prof Dominic Ng | University of Queensland

Charcot, supported by Fat Rabbit

The numerous proteins linked to ALS share the interesting ability to behave like a liquid inside cells. When proteins behave like this, we call them protein condensates. Imagine these protein condensates as very much like the blobs in a lava-lamp. The blobs move around, break apart and can join up with other blobs seemingly at random and this behaviour is required to keep motor neurons healthy. Recently, we discovered that a subtle drop in pH, a measure of acidity or alkalinity, inside cells prevents the formation of protein condensates. This is significant as there is a gradual decrease in pH (acidosis) in our brains and spinal cords as we age and this coincides with the emergence of disease. Our study aims to determine whether this decreased pH changes the normal liquid behaviour of ALS proteins to trigger abnormal protein behaviour that can cause the loss of motor neurons. Our findings will help us better understand the early molecular triggers of disease and spur research in pH modulation as new treatments.

Image of Dr Abigail Pfaff | Murdoch University
Dr Abigail Pfaff | Murdoch University

Paul Brock MND Research Grant

Mobile DNA or ‘jumping genes’ make up nearly half of a person’s DNA and can affect how cells function. Some of these pieces of mobile DNA are more active than others and their increased activity has been identified in people with motor neuron disease (MND). Pieces of mobile DNA are large and repeat themselves throughout a person’s DNA which make them difficult to study with current techniques. However, a new type of technology will allow us to analyse these pieces of mobile DNA in more detail and with greater accuracy. We will use this data to identity the specific pieces of mobile DNA that are the most active in people with MND. We hope to generate a mobile DNA signature to identify those people who have the most active mobile DNA and could potentially benefit from treatments available to reduce this activity.

Image of Dr Andrew Phipps | University of Tasmania
Dr Andrew Phipps | University of Tasmania

Jenny Simko MND Research Grant

In MND, motor nerve cells become hyperactive, which causes the release of molecules that become toxic to the nervous system. Some nerve cells are particularly sensitive to breaking down as a result of this toxic environment. The long nerve fibres that connect nerve cells and our muscles are also targets for this breakdown, which may trigger independently from the rest of the motor nerve cells. Protecting nerve cells from breaking down is dependent on protecting both the cell body itself, as well as their long fibres. We have identified a range of changes that occur to the nerve cell fibres that contribute to their breakdown after nerve cells become hyperactive. We seek to understand these changes further, and aim to counteract the changes to prevent the fibres from degeneration in MND. This project will test molecules to prevent nerve fibre break down in MND and provide a pathway to preclinical drug development for MND.

Image of Dr Eduardo Albornoz | University of Queensland
Dr Eduardo Albornoz | University of Queensland

Murray Geale MND Research Grant

Our project aims to develop a new "brain in a dish model" for studying MND. Using blood cells from people living with MND, we generate microglial cells—the brain’s immune cells—and combine them with lab-grown brain-like structures (organoids) derived from stem cells. This advanced “mini-brain” system will allow us to test potential treatments in a way that closely mimics the conditions of the human brain. By focusing on immune pathways involved in inflammation and nerve damage, we aim to identify more effective and precise therapies for MND. Ultimately, this research could lead to a more personalised treatment approaches.

Image of Dr Grant Richter | Macquarie University
Dr Grant Richter | Macquarie University

Ian Sneddon Two Rivers Run MND Research Grant

In almost all MND patients, a protein called TDP-43 becomes dysfunctional, failing to process RNA properly as it does in healthy individuals. This dysfunction disrupts critical cellular processes eventually leading to the formation of toxic protein aggregates. This project will investigate how a specific protein modification, called phosphorylation, may drive early changes to TDP-43’s ability to bind RNA and contributes to disease progression. To achieve this, we will first use neurons grown in the lab to examine how phosphorylated versions of TDP-43 interact with RNA. Next, we will use our unique transparent zebrafish model to see phosphorylated TDP-43’s effect in living motor neurons. By uncovering how these early changes lead to disease, we will identify new targets for delaying or altering the course of MND, providing hope for better treatments.

Image of Dr Lotta Oikari | QIMR Berghofer
Dr Lotta Oikari | QIMR Berghofer

NTI MND Research Grant

People with ALS have abnormal aggregation of a protein called TDP-43 in brain cells, contributing to disease progression. Recent research suggests that TDP-43 may also affect the function of the blood-brain barrier (BBB), which is a crucial defence system located in the blood vessels of the brain. How TDP-43 affects the BBB in ALS is not well understood. Here, we will use human stem cells, obtained from people with ALS to generate laboratory models of the BBB to investigate the role of TDP-43. We will investigate if abnormal TDP-43 in ALS leads to breakage of the BBB, leading to increased leakage of substances into the brain and whether this leads to increased inflammation in the brain. Understanding this relationship could help better understand ALS progression and develop new treatments for ALS.

Image of Dr Neville Ng | University of Wollongong
Dr Neville Ng | University of Wollongong

MonSTaR MND Research Grant

There is no cure and few effective treatments for Amyotrophic Lateral Sclerosis (ALS). ALS is caused by degeneration of motor neuron terminals from skeletal muscle and motor neuron death. Use of stem cells converted from patient skin or blood can replace obtaining human motor neuron terminals directly from patients. This project aims to find drugs that can reduce denervation and prolong motor neuron survival with a robot-assisted stem cell neuro-muscular junction screen, and potentially slow the progression of ALS. 

Image of Dr Nirma Perera | University of Melbourne
Dr Nirma Perera | University of Melbourne

The Elizabeth and Peter John Cahill MND Research Grant

Traditionally, the focus in MND has been on dying nerve cells. However, the unsung heroes of the nervous system are called “glial cells”, which provide nerve cells essential functional support. We will examine how a type of glial cells called “astrocytes” handle waste through a process named autophagy. Our preliminary findings indicate that astrocyte autophagy waste clearance is overactive in MND. Using transgenic mouse models, we will normalize this process, thereby making astrocytes provide better support to nerve cells, helping them live healthier and thereby longer. Outcomes will help us better understand causes and guide new treatments for MND.

Image of Dr Rita Mejzini | Murdoch University
Dr Rita Mejzini | Murdoch University

Peter Stearne Familial MND Research Grant

Everyone has two FUS gene copies, if one copy carries a mutation, patients are affected by MND. An existing therapeutic reduces all copies of the FUS gene. We have developed therapeutics that target only the mutant copy, stopping the production of toxic protein and allowing normal FUS protein to be produced to fulfil its functions. We have also developed a therapeutic that reduces all FUS but has a different mechanism of action and chemical properties that improve safety. This project will examine the effects of our therapeutics on neuronal health and function in motor neurons grown from FUS-ALS patient cells.

Image of Dr Saravanabavan Sayanthooran | Macquarie University
Dr Saravanabavan Sayanthooran | Macquarie University

Daniel Veysey MND Research Grant

While ALS can be inherited, environmental factors are believed to play a key role in determining who develops the disease and how it progresses, especially in sporadic cases. This is evident in identical twins: despite sharing the same genes, only one may develop ALS. Identifying these environmental triggers has been challenging because traditional studies often rely on questionnaires and patient records, which have significant limitations. This project takes a fresh and innovative approach. By employing a novel assay in an innovative way, it will begin systematically investigating how environmental and workplace factors contribute to both sporadic and familial ALS. At the same time, it aims to lay the groundwork for exploring how genes and the environment interact, setting the stage for uncovering the mechanisms behind these processes. This work could provide valuable new insights and accelerate progress in understanding and reducing the risk of ALS.

Image of Dr Sonam Parakh | Macquarie University
Dr Sonam Parakh | Macquarie University

Col Bambrick MND Research Grant

There is an urgent need for new MND treatments. This proposal explores a novel strategy using drugs that target the electrical properties of motor neurons, the cells affected in MND. These properties are critical component of the brain's communication system because they regulate nerve activity. We will examine whether these drugs are protective in human cells and mice that develop MND: the first step in their development for MND patients. Our approach is exciting because these drugs are ‘repurposed’, meaning they are already on the market for other conditions. This will expedite their development as a new treatment for MND.

Image of Natalie Grima | Macquarie University
Natalie Grima | Macquarie University

Superball XVII MND Research Grant

We have identified a subgroup of sporadic MND patients with a unique molecular signature in the cerebellum, a brain region with a lesser-known role in MND. Interestingly, this subgroup demonstrates the same pattern of hallmark TDP-43 pathology as MND patients who carry a mutation in the C9orf72 gene. We aim to uncover whether this sporadic MND subgroup, encompassing around one-third of all MND cases, shares other similarities with C9orf72-linked MND. Identification of similar genomic (DNA) or transcriptomic (RNA) signatures means that individuals belonging to this sporadic MND subgroup may have common therapeutic targets to the major genetic cause of MND

Image of Prof Peter Catcheside | Flinders University
Prof Peter Catcheside | Flinders University

Eileen Grace Bignall MND Research Grant

This project will bring together people living with MND, their carers, clinical care teams, sleep scientists and engineers to refine and test a new mattress sensor device that will measure breathing in more detail that has previously been possible. This will allow breathing problems and sleep to be routinely assessed in the home without any intrusive worn sensors. Co-design and pilot tests through this 1-year project will accelerate translation into more comprehensive and streamlined respiratory-sleep medical care for people with MND.

Image of Rebecca Franics | Flinders University
Rebecca Franics | Flinders University

MND South Australia MND Research Grant

Research has found that up to 50% of people living with MND may experience cognitive and behavioural changes as part of the disease. Currently, we don’t know how families, who are experiencing MND, would prefer to learn about and manage cognitive and behavioural changes. This means that the ways we currently assess for and manage cognitive and behavioural changes are inconsistent, or it may even mean that these changes are not detected or discussed at all. The Flinders University team of researchers, who work in the MND space, will partner with people with MND and their families, to determine ways that they would prefer to learn about and manage cognitive and behavioural changes. The research team aim to understand what suits everyone in the family and how care can be optimised to meet their needs. The outcomes of this research project will help to develop clinical frameworks and educational resources for people with MND, their families and MND clinicians. These resources will support families to work together with their health care team to navigate cognitive and behavioural changes, in ways that best suit their individual needs and preferences.
 

Image of Yuval Gurfinkel | Murdoch University
Yuval Gurfinkel | Murdoch University

Linda Elphick MND Research Grant 

In SOD1-linked MND patients, as well as many sporadic MND cases, the SOD1 protein folds incorrectly, forming toxic aggregates that interfere with normal neuronal functioning. In this project, we will compare the genetic profiles of people with MND and healthy individuals in cells taken from a skin biopsy and use these cells to test the effect of our SOD1 suppression therapy. The findings will allow us to rapidly identify sporadic patients with genetic profiles that resemble SOD1-linked cases who may benefit from SOD1 suppression in future clinical trials, making our anti-SOD1 drug widely accessible to MND patients.

MNDRA PhD Scholarship Top-up Grants

Lead investigator: Flora Cheng
Institution: Macquarie University
Title: Identification and characterisation of RNA-protein interaction in pathological aggregates of TDP-43 in MND

Amyotrophic lateral sclerosis is a devastating motor neuron disease without any cure to date. The proposed research will determine whether mutation in an important protein found in aggregates in ALS patients, TDP-43, exhibit altered RNA binding properties which leads to the formation of aggregation in cells. This could be a critical piece of information to a potential RNA-based therapeutic treatment to either reverse or prevent formation of those TDP-43 inclusions in ALS patients.

Lead investigator: Stephanie Howe
Institution: University of Queensland
Title: Characterising the spatio-temporal landscape of neuroinflammation and metabolism in ALS

Metabolic changes and neuroinflammation are some of the many pathways associated with worsening pathology in MND. Unfortunately, the sequence of events leading to neuronal death and the spread of disease require further elucidation. My PhD aims to use a variety of human clinical samples and data, mouse models and in vitro cell models of MND to help understand how inflammation contributes to metabolic changes and vice versa. My goal is to identify specific mechanisms of MND cell pathology and death, and to establish appropriate models for recapitulating the complex landscape of this disease.

Lead investigator: Andrew Quattrocchi
Institution: The University of Melbourne
Title: Understanding and modelling the neurovascular niche in health and MND

The health of our brain depends on the health of its blood vessels. In MND we know motor neurons that reside in the brain are uniquely vulnerable. What we do not understand is how the 640km of blood vessels in our brain which supply all our nutrients and oxygen, but also removes waste, may contribute to this motor neuron death. This project aims to comprehensively characterise vascular and neural changes in MND, using patient derived 3D human stem cell systems. By understanding how and what goes wrong in our blood vessels, this project is poised to inform a new generation of therapeutic strategies that targets both our vascular and brain health.

Lead investigator: Elise Kellet
Institution: Queensland Brain Institute, University of Queensland
Title: The role of post-translational modification of TDP-43 in disease pathology

MND is characterised by the aggregation of proteins in upper and lower motor neurons. The main aggregating protein experiences different chemical changes in disease. While initially believed to drive disease progression, recent findings question whether these changes may instead be protective. My research investigates the role of chemical alterations of this protein in disease pathology by identifying upstream proteins that regulate the alterations and exploring downstream consequences. My aim is to improve our understanding of MND pathology and identify new processes for therapeutic targeting to help people living with MND.

Lead investigator: Kathryn Maskell
Institution: University of Tasmania
Title: Do upper and lower motor neurons need different treatments to effectively stop neurodegeneration in ALS?

ALS involves degeneration of both the upper motor neurons in the brain and lower motor neurons in the spinal cord, but we still don’t understand how degeneration starts and spreads between them. Upper and lower motor neurons have different characteristics and reside in different environments, new evidence suggests that they are differentially vulnerable to disease mechanisms in ALS. Importantly, the two populations may need different therapeutic support to prevent disease progression. This research aims to interrogate the vulnerabilities of upper and lower motor neurons to disease mechanisms of ALS and will inform our approach to treating patients suffering from ALS.

Lead investigator: Aida Viden
Institution: University of Melbourne
Title: Investigating the anatomical origins of MND

MND is caused by the death of both brain and connecting spinal motor neurons (MNs). Importantly, transmission of disease amongst MNs propagates in a cascade. Our current understanding of the mechanism and direction of pathological spread between brain and spinal MNs is limited. This PhD project aims to determine the primary site of disease initiation in MND with the use of a gene-editing approach targeting brain and spinal MNs individually in a clinically relevant MND mouse model. By understanding which MNs transmit disease and how, we can inform new therapeutic interventions targeting brain and/or spinal MNs to prevent further spread.

Currently funded multiyear grants from previous years

Lead investigator: Dr Chien-Hsiung (Alan) Yu
Institution: University of Melbourne
Title: Investigating TDP-43-associated immune activation to map the causes of MND

Lead investigator: Dr Rachel Atkinson
Institution: University of Tasmania
Title: Freezing MND in its tracks

Lead investigator: Dr Nicole Sheers
Institution: University of Melbourne
Title: Developing a new exercise therapy to improve breathing and cough in people living with MND

Lead investigator: Dr Thais Sobanski 
Institution: The University of Queensland  
Title: Boosting sugar breakdown to halt the progression of MND 

Lead investigator: Dr Thanuja Dharmadasa
Institution: University of Melbourne and The Florey
Title: Exploring disease heterogeneity across MND clinical phenotypes using a multimodal, multicentre neuroimaging approach

This long-term study will build an integrative national network to use advanced brain neuroimaging and detailed clinical assessments to follow patients through their disease journey and identify different clinical subgroups. It is hoped this will significantly increase our understanding of disease mechanisms and develop imaging markers that can differentiate the MND subtypes. For people living with MND, this research will lead to better prediction of disease progress and spread, earlier as well as more specific implementation of management and treatment strategies. This knowledge can also inform the future design of clinical trials for the development of targeted treatment strategies.

The recipients of the Daniel McLoone Major Research Initiative are jointly funded by MND Research Australia (MNDRA) and FightMND.

Lead investigator: Professor Bradley Turner
Institution: University of Melbourne and The Florey
Title: Australian Preclinical Research ALS (APRALS) Network: a roadmap for effective translation of therapeutics for sporadic MND

This project will launch Australian Preclinical Research ALS (APRALS), a national collaborative network which aims to accelerate development of novel treatment candidates towards clinical trials in MND. The network will bring together distinct and advanced expertise in human stem cell technology and animal models of MND to develop a novel class of powerful DNA designer drugs targeting key aspects of sporadic MND. By targeting these key aspects of sporadic MND, the researchers will significantly improve the ability to translate findings in animal and human models of MND into the clinic. It is hoped APRALS can provide a rich pipeline of promising treatment candidates for clinical trials applicable to the majority of people living with MND.

The recipients of the Daniel McLoone Major Research Initiative are jointly funded by MND Research Australia (MNDRA) and FightMND.

Lead investigator: Dr Jeremy Lum
Institution: University of Wollongong
Title: Identifying drivers that contribute to the loss of neuronal connections in the early stages of ALS

Motor neurons contain important extensions used to form connections with other neurons and muscles. One of the earliest changes in ALS are the degeneration of these extensions, leading to an inability to effectively communicate, ultimately causing to paralysis. This project will focus on identifying the disrupted biological networks that lead to the loss of these extensions and look to find therapeutic targets to restore these connections in patient-derived cells and animal models of ALS.

Lead Investigator: Dr Alison Hogan
Institution: Macquarie University 
Title: The RNA-binding protein SFPQ offers a novel avenue to understand disease mechanisms and identify therapeutic targets in MND

Dysregulation of a new protein, SFPQ, has recently been linked to MND, presenting an exciting new opportunity to understand disease biology from a fresh perspective. This project will be among the first in the world to examine how SFPQ interacts with other key MND proteins and how these interactions contribute to disease progression. This will provide insight into disease biology and offer a new direction to identify novel interactions and targets for therapeutic modification.