Neurological & Central Nervous System


The central nervous system consists of the brain and spinal cord. It regulates and coordinates body activities. If neurons are damaged, the result is often a diagnosis of Parkinson’s disease, motor neurone disease, stroke or multiple system atrophy. Read on to find out more about these conditions and what NeuRA is doing to understand, treat and cure them.


Breathing is a complex motor task that needs to be coordinated at all times while we eat, speak, exercise and even during sleep. Our overall goal is to determine the role of neural drive in impairments of respiratory muscle function in older adults (over 65 years), people with chronic obstructive pulmonary disease (COPD), spinal injury or obstructive sleep apnoea (OSA).

Motor neurone disease

Motor neurone disease (MND) is a neurodegenerative disease that causes rapidly progressive muscle weakness. Specifically, the disease affects nerve cells (motor neurons) that control the muscles that enable you to move, speak, breathe and swallow. The precise cause of MND and its disease process remains a complete mystery. Some researchers are looking into possible environmental triggers – such as exposure to toxins or electrical injury.

Multiple system atrophy

Multiple system atrophy (MSA) is a progressive degenerative neurological disorder that affects adult men and women, usually in their 50s or 60s. It is caused by degeneration or atrophy of nerve cells in specific areas of the brain. The cause of MSA is unknown, no specific risk factors have been identified, and there is no cure or effective treatment. Treatment for MSA includes medications and lifestyle changes to help manage symptoms. The condition progresses gradually and eventually leads to death.

Parkinson’s disease

Parkinson’s disease is a progressive, degenerative brain disease that causes trembling, stiffness, slowness of movement and a loss of fine motor control. The disease destroys neurons in an area of the brain called the substantia nigra. Without these dopamine-producing cells, the brain’s ability to control movement is progressively reduced. We are conducting research to improve diagnosis of Parkinson’s disease and gain a better understanding of the mechanisms that cause the disease. Symptoms Symptoms of Parkinson’s disease are caused by a gradual deterioration and death of brain cells in the substantia nigra. However, people with Parkinson’s can lose up to 70% of susceptible brain cells and go on for many years before symptoms become noticeable. While symptoms vary from person to person, the most well-known symptom is a tremor. People with Parkinson’s disease may also experience slowness of movement, stiffness, a loss of automatic movements such as blinking and smiling, changes in speech and, in the later stages of the disease, dementia.


Over 60,000 Australians suffer a stroke every year, making it the second most common cause of disability in Australia. More than half of those who survive a stroke require help with normal daily activities. There is no cure for stroke, nor any forthcoming. Rehabilitation is the only method to recover movement of stroke-affected limbs. Our research focuses on the recovery of movement after stroke. We are currently setting up a project to test the delivery of rehabilitation therapy via high speed broadband to people in regional and remote parts of Australia. We are also making detailed assessments of stroke patients before and after rehabilitation that will allow us to predict which patients will benefit most from therapy.

See what’s going on at NeuRA


Parkinson's disease

Investigating whether SNCA genetic variation relates to pathological variation in Parkinson’s disease Mutations in the SNCA gene (encoding alpha-synuclein) cause autosomal dominant forms of Parkinson’s disease. This project aims to determine whether generic variation in SNCA relates to pathological severity of inclusion pathologies and alpha-synuclein protein levels. With Dr Scott Kim (SRO) The major focus of these projects is to understand the role of lipid dysfunction in Parkinson’s disease and the related disorder of multiple system atrophy. Increasing evidence shows that lipids regulate a number of neurodegenerative processes. Understanding the role of lipids in alpha-synuclein aggregation process in parkinsonian syndromes We have recently produced compelling evidence showing that lipid levels are significantly altered in disease-affected regions of parkinsonian syndromes. This project aims is to determine how lipids regulate alpha-synuclein aggregation process in parkinsonian syndromes. Determining the role of COQ2 in multiple system atrophy pathogenesis Myelin is a specialised lipid membrane that encases the axons of all neurons in the brain and is made by oligodendrocytes. These cells do not properly make myelin and degenerate in certain brain regions in multiple system atrophy. Without myelin neurons eventually die. Genome-wide association studies indicate that COQ2 is associated with an increased risk for multiple system atrophy. The aim of this project is to determine the role of COQ2 in the pathogenesis of multiple system atrophy. With Dr Nicolas Dzamko (RO) The major focus of these projects is to understand how mutations in certain genes cause inherited forms of Parkinson’s disease and whether/how these genes also contribute to non-inherited (sporadic) Parkinson’s disease. A particular focus is on leucine-rich repeat kinase 2 (LRRK2), a promising therapeutic target for Parkinson’s disease. Measuring LRRK2 by flow cytometry The LRRK2 protein is highly expressed in white blood cells. The aim of this project is to establish a flow cytometry assay to measure LRRK2 protein in white blood cells from Parkinson’s disease patients. This assay could then be used to monitor LRRK2 in any clinical trials using drugs to block LRRK2 function. Effect of LRRK2 mutations on PD-associated inflammation Inflammation is a common feature of Parkinson’s disease and LRRK2 is involved in the regulation of inflammation. This project aims to measure inflammatory markers in the serum and cerebrospinal fluid of subjects that have LRRK2 mutations but not yet Parkinson’s disease. We will determine if inflammation occurs early in the disease process and whether certain inflammatory markers can be used to predict Parkinson’s disease before clinical symptoms. LRRK2 expression in brain LRRK2 is promising drug target for the treatment of Parkinson’s disease. This projects aims to understand what happens to LRRK2 in the brain of Parkinson’s patients. This information will aid drug development and clinical trials for LRRK2 inhibitors. LRRK2 and idiopathic Parkinson’s disease Pathogenic mutations in LRRK2 cause inherited Parkinson’s disease but polymorphisms in LRRK2 are also a risk factor for sporadic Parkinson’s disease. This project aims to measure LRRK2 protein and its function in sporadic Parkinson’s disease patients. Results from this work will help determine if LRRK2 blocking drugs will be beneficial for all forms of Parkinson’s disease. LRRK2 and type-1 interferon We have established that LRRK2 is involved in inflammatory pathways that regulate interferon production. This project will generate and utilise state-of-the-art cellular models (induced pluripotent stems cells and crispr/cas9 genome editing) to understand how Parkinson’s disease-causing LRRK2 mutations affect inflammation. TLR2 and the pathological spread of alpha-synuclein The accumulation of insoluble alpha-synuclein protein is a hallmark feature of brain tissue from Parkinson’s patients. Recent evidence suggests that alpha-synuclein may spread through the brain in a prion-like manner, contributing to neurodegeneration. This project aims to determine the contribution that the toll-like receptor 2 (TLR2) makes to the spread of alpha-synuclein through the brain. The association of VPS35 and pathological alpha-synuclein Mutations in VPS35 are a rare cause of inherited Parkinson’s disease. Recent evidence suggests that VPS35 mutations may contribute to the accumulation of alpha-synuclein protein. This project aims to determine the association between VPS35 and alpha-synuclein in human Parkinson’s disease brain and to use cellular models to define this relationship. Implications of neuronal toll-like receptor activation for Parkinson’s disease Neuroinflammation contributes to cell death in Parkinson’s disease but how and via which pathways is mostly unknown. This project uses cell models to determine the contribution of the major inflammatory regulating toll-like receptor (TLR) pathway to neuroinflammation, with a particular focus on the largely unexplored role of TLR signalling in neurons.