Dementia: when do I know I have a problem, and what is happening in my brain?

Dr James Burrell is a Senior Research Officer and clinical neurologist whose research interests lie in linking clinical symptoms and pathology in dementia syndromes.

Dr James Burrell

Dr James Burrell

In my work as a clinical neurologist, I often encounter people who are concerned that they might be developing the dreaded d-word: dementia. They report being more forgetful than previously, forgetting the names of people, places or things, or perhaps just not feeling as ‘sharp’ as they once did. In my experience, these sorts of concerns are common. Importantly, however, only a proportion of people with such symptoms actually go on to develop dementia.

Working out who will develop dementia, and more specifically which type of dementia will be developed, is one of the major challenges cognitive researchers and clinicians face. We are presented with two separate, but related problems: first, how can we tell when minor forgetfulness heralds the onset of something more serious? Secondly, if someone has an obvious dementia, how can we make an early and accurate molecular diagnosis?

We know from many well-designed studies that neurodegenerative disorders begin years before any symptoms develop, and that to be effective a treatment will most likely need to start at the very earliest stages, before any significant and permanent damage develops. On the other hand, not everyone with mild cognitive symptoms actually progresses to develop dementia. Being able to accurately identify patients at risk of developing dementia at a very early stage is one of the major goals of research in neurodegenerative diseases.

In the Frontier clinic based here at NeuRA, we are often faced with the opposite problem: we assess patients with early dementia who present with memory, language, or behavioural disturbances, but it can be difficult to work out the specific underlying brain disease. In many ways, our research aims to bridge this gap between the problems related to ageing that people face in their everyday lives and the physical changes in the brain that are ultimately responsible. We use a combination of methods, including detailed clinical assessment, neuropsychological or cognitive testing, sophisticated brain imaging, neurophysiological techniques, gene testing, and even blood and tissue biomarkers, to try and better link cognitive symptoms and specific brain diseases. With collaborators in the UK we have even developed a new app, for cognitive testing in clinical practice (ACEmobile™ for iPad, available from the Apple App Store). Only after we can make an early and accurate diagnosis of a neurodegenerative brain disorder will the hunt for a meaningful treatment really forge ahead.

Contracture: understanding mechanisms and testing treatments

As part of a new National Health and Medical Research Council Program Grant on motor impairment, Prof Rob Herbert aims to advance the transfer of new understanding of physiology and pathophysiology in motor impairment toward the clinical outcome of improved motor function.

Prof Rob Herbert

Prof Rob Herbert

Motor impairment is a common consequence of a number of illnesses and injuries. One type of motor impairment that is an important cause of physical disability is muscle contracture. A contracture is a stiffening of the muscles that limits normal joint movement, and severe contractures cause deformities that are the most visible manifestation of brain damage. Contractures arise when brain lesions, including those that arise from stroke or traumatic brain injury, cause paralysis or spasticity. Paralysis and spasticity change the mechanical environment of muscles – that is, they cause muscles to experience different patterns of activity, different changes in length and different forces than would normally be experienced. The muscles adapt in response to their altered mechanical environment by becoming stiffer, causing joints to become less mobile.

Contracture is a common problem. In a recent study, my colleagues and I monitored 200 consecutive people admitted to a Sydney hospital with the diagnosis of stroke. Six months after admission, half of all those people had developed at least one contracture. Contractures are also common in people with many other sorts of brain lesions. For example, contractures are prevalent in people who have had a traumatic brain injury, or who have multiple sclerosis or cerebral palsy.

Contractures prevent joint movement, so they cause physical disability. For example, many people who have had a stroke or traumatic brain injury develop contractures of the calf muscles. Calf muscle contractures impede ankle motion, making it difficult to stand up from a chair or walk normally. In the same way, contractures of shoulder muscles can impair the ability to reach and contractures of wrist and finger muscles can impair grasp. Severe muscle contractures can cause the limb to adopt a fixed position. For many people, contractures become a much greater impediment to normal movement than the paralysis or spasticity that initially caused the contracture to develop.

There has been surprisingly little research into the mechanisms of contracture. As a result, the mechanisms are poorly understood. Studies on animals have shown that it is possible to make muscles become short or stiff with a number of experimental procedures. For example, leg muscles can be made short by immobilising the leg in a plaster cast, and diaphragm muscles can be made short by inducing emphysema (a lung disease). These studies show that the stiffening of muscles can occur either because of changes in the muscle tissue (the muscle “fibres” or “fascicles”), or because of changes in the tendons that join muscle fascicles to bones. But studies on animal muscles can’t tell us about the mechanisms of contractures seen in human populations. Surprisingly, it is still not clear whether contractures in people who have had a stroke or traumatic brain injury are due to changes in the muscle fascicles or tendons.

There is just as much uncertainty about how to prevent and treat contracture. For the last half-century, physiotherapists and nurses have applied stretches to muscles, or passively moved limbs, or applied splints or casts to stretch the limb, with the aim of preventing or treating contractures. But recent research suggests these interventions have little effect. For example, in one study, 63 volunteers who had experienced a stroke were randomly allocated to receive either a wrist splint or no splint. Two months later there was no discernable difference in the stiffness of the wrist of people who had or had not been splinted. There have now been over 35 studies like these, and they quite consistently show little or no effect of stretch or movement-based interventions. For now at least, there are no treatments that have been clearly shown to prevent or reverse contracture.

Eventually, scientific research will provide answers, both about the mechanisms of contracture, and about how to prevent and treat contracture. The first steps have been made in identifying the abnormalities of gene expression that are ultimately expressed as contracture. New ideas for treatments are being generated by basic research, for subsequent testing in clinical trials. Our motor impairment program will study human volunteers and patients to learn more about normal motor function and the mechanisms of motor impairment, and to test the clinical efficacy and mechanisms of novel treatment interventions. The development of new techniques for imaging and measuring the internal architecture of muscles using MRI provides one promising advance. One study will look at how muscle tendons and fascicles are recruited during movement, which will inform subsequent clinical studies in people in whom contracture is common, such as people with stroke, spinal cord injury and multiple sclerosis.

Hopefully, the next decade will see major advances in both our understanding of the mechanisms of contracture and how to treat them.

An example of one of the unique muscle images generated by Prof Herbert's team. In the centre is a human leg muscle. The blue lines show the course of muscle cells in six locations in the muscle. The insets provide information about how the cells terminate on the tendinous sheets that cover the upper and lower surfaces of the muscle.

An example of one of the unique muscle images generated by Prof Herbert’s team. In the centre is a human leg muscle. The blue lines show the course of muscle cells in six locations in the muscle. The insets provide information about how the cells terminate on the tendinous sheets that cover the upper and lower surfaces of the muscle.

An international approach to tackling Parkinson’s disease

Dr Nic Dzamko and Prof Glenda Halliday have put together an international team dedicated to researching the causes of Parkinson’s disease. They will be the first in the world to use valuable early clinical samples to identify the genetic and molecular underpinnings of this brain illness.

Parkinson’s disease is a debilitating neurodegenerative disorder with no current cure. 1 in every 30 Australians is diagnosed with Parkinson’s disease, and these numbers are predicted to rise. Over the last 10-15 years, it has emerged that genes play an important role in the risk of developing Parkinson’s disease. Approximately 16 genes have now been identified that increase the risk of developing Parkinson’s disease. Understanding what these genes do in the healthy brain, and how their functionality might go wrong, has become a major focus in the search for clues about the cause of this disease.

Dzamko2

Dr Nic Dzamko in the laboratory

One of these genes, called LRRK2, has received considerable attention. The LRRK2 gene encodes a protein that belongs to a class of enzymes called kinases, which is interesting to researchers because many anti-cancer drugs developed by the pharmaceutical industry also act by blocking kinases. In the past few years, more than 20 drugs that can block the kinase LRRK2 have been patented. While it is hoped that these drugs may be beneficial for the treatment of Parkinson’s disease, more work needs to be done to understand exactly what LRRK2 does, and therefore whether drugs that block its action will be safe and therapeutically useful. To better understand the function of LRRK2, our team at NeuRA has initiated two new projects in collaboration with scientists from around the world.

The first project involves us leading a group of scientists from London, Tokyo, California and the Netherlands. Using 400 samples that have been sent to us from these locations, and that cover a range of brain regions at different disease stages, we will determine if, when and where the expression of the LRRK2 enzyme goes wrong in the Parkinson’s brain.

The second project aims to investigate the idea that inflammation is linked with Parkinson’s disease, in collaboration with researchers in the US and Europe. This project is particularly exciting, as it may identify much-needed markers of early disease. By working with the worldwide LRRK2 Cohort Consortium, established by the Michael J Fox Foundation for Parkinson’s Research, we have access to more and better samples to ultimately obtain more meaningful data. We will measure a range of biological markers associated with inflammation in serum and cerebrospinal fluid. By comparing the extent and type of inflammation in people who do and do not have certain genetic mutations, and between people with Parkinson’s disease and healthy controls, we will identify whether inflammation is an early sign of Parkinson’s disease. This world-first access to blood samples from people with a large genetic risk of getting Parkinson’s, but who do not yet have the disease symptoms, is a chance to try and identify potential treatments for the early stages of this illness.

These projects have taken about a year and over 300 emails to come together. Although meetings are often scheduled in the very early hours of the morning to accommodate time zones, working together as an international team to leverage skills and resources is an important step toward solving the problem of Parkinson’s disease. Of course, our work would not be possible without the funding we have received for these projects from the Michael J Fox Foundation and the Shake it Up Australia Foundation.

Reasons to run

This Sunday, August 10, the Sydney City2Surf will include two groups of people who have more reasons than many to get up early and run to Bondi beach.

Evan Brownsmith is organising a team of eager accountants from PKF Lawler Tamworth and Walcha, NSW to run the City2Surf in support of motor neurone disease (MND) research.

PKF team cropped

The PKF Lawler team: (L – R) Blair Richards, Kelee Hawker, Evan Brownsmith, Michelle Higgerson and Nicole Parkinson

This terrible disease has recently been diagnosed in two of PKF Lawler’s longstanding clients, with a profound impact upon their families and friends and the whole team at PKF Lawler. Through our efforts, both running and fundraising, we hope to raise awareness in the Tamworth community of the impact of MND. By partnering with NeuRA we hope to provide valuable funds for the development of life-altering treatments for MND sufferers.

Like most people, I have a love-hate relationship with running. On a good day – when there is sun and very little wind, and it’s not too hot and not too cold, and you’re feeling fit and your legs feel strong, and you’re wearing the right outfit, and the scenery is good, and no-one is watching you, and you’ve got a really good album playing in your ears – running is the best thing in the world! There’s nothing better than the sense of achievement you get from pushing yourself further as your feet pound the pavement. On every other day, running sucks!!

Most of the time, running is really hard! That’s why we come up with so many excuses for not doing it. We like the idea of running, but often we don’t enjoy running itself. What we don’t think about each time we choose not to run, though, is how lucky we are to be able to run. Most sufferers of MND will lose the ability to run. This is the inspiration for team PKF Lawler in the City2Surf, and this is what motivates me to get off the couch, put my joggers on and make the most of my good health and good fortune.

For those who don’t know, MND is the name given to a group of diseases in which the motor nerve cells (neurons) controlling the muscles that enable us to move, speak, breathe and swallow, undergo degeneration and die. Motor function is controlled by the upper motor neurons in the brain that descend to the spinal cord; these neurons activate lower motor neurons, which exit the spinal cord and directly activate muscles. With no motor neurons to activate them, muscles gradually weaken and waste away. These effects are irreversible, and as MND sufferers progressively lose function, their quality of life is diminished and independence is undermined.

On August 10 this year my colleagues and I hope to make a significant difference for these people. We cannot directly improve the lives of MND sufferers, nor can we make it easier on their families. We cannot hope to cure this terrible disease ourselves, but we know that our modest contribution to NeuRA will help the very people who just might. Perhaps more importantly, through demonstrating a willingness to ‘give it a go’, we are setting a great example to the community of Tamworth. We want to show that it’s important to get out there and have a crack, not because we should, but because we still can.

Fundraising stall

Ashlee Schwennesen and Julianne McDougall raising funds with a fresh produce stall

You can donate to the PKF Lawler team here.

 

Simone Riley is participating in the City2Surf with her family to support stroke rehabilitation research and to honour her Dad, a proud City2Surfer.

dad and me

On July 21, 2013, my Dad, a man who lived a healthy, active, and happy lifestyle, was stopped in his tracks by unfortunate genetics and a nasty stroke.

A man who was 64 years young, who had run 20+ City2Surfs (his favourite event) and over 60 marathons, trekked in Nepal and to the top of Mt Kilimanjaro, and was training for a trek from France to Spain, Dad was now in for the biggest challenge yet. His was an atypical stroke, meaning that he didn’t suffer the ‘usual’ deficits in movement that stroke often inflicts, but he did lose his vision and began to experience major cognitive and memory deficiencies.

Simone’s dad in Nepal

As Dad’s hospital days turned into weeks, and then months, our hope went up and down like the rollercoaster going on in Dad’s head. On my first visit to the hospital, I walked into a dark room and was faced with a body on a mattress on the floor that was heavily sedated, as the hospital staff didn’t know what else to do! When Dad woke up every now and then, to walk and eat, our hearts broke when he didn’t recognise me, or even my Mum, his wife of 43 years! Thankfully, we found a Brisbane doctor who agreed to come to the Gold Coast to assess him. This was the first hope we had. After moving hospitals, adjusting his medication, and some wonderful rehabilitation, physiotherapy, and speech therapy, we gradually saw the man who ‘once was’ slowly coming back. He once again knew who Mum was, who I was, and also recognised his other daughters, his son, his grandkids, and other people important to him. After almost six months in hospital, my dad walked out with my mum and went home.

The start of his (and her) new lives involved major adjustments; Mum was now his full time carer and also unfortunately had to take on the role of rehabilitator. I felt compelled to do and find what I could to help them with the struggle to find appropriate post-hospital rehabilitation.

While researching stroke, I stumbled across NeuRA. What better way to honour my Dad than to join the NeuRA City2Surf team and make him proud; to run his favourite event, while raising much-needed funds for a charity that will continue research into stroke rehabilitation and one day perhaps even prevent stroke altogether?

It has almost been a year since Dad’s stroke. Things are far from perfect; he has good days and bad days. Only last week, when I sat holding his hand on the couch, he knew I was there, but couldn’t, for all his wanting and trying, get my name out. His vision will never come back, but through trial and error and ups and downs he is rising, admirably, to his challenges.

pb marathon

This year, along with my sister, my best friend (who is like Dad’s fourth daughter), my Mum, some cousins and lots of Dad’s friends, Dad will once again take the trip to Sydney to run/walk/shuffle/crawl/hop/skip/jump; in short, do whatever it takes to complete his annual City2Surf! Given that Dad really doesn’t like the fact that he missed it last year, participating in this year’s race is in itself an achievement that we will all enjoy, almost as much as the cold beer we share with him at the finish line.

You can donate to Simone’s fundraising effort here.

You can also donate to the 2014 NeuRA Runners team here.

The life of an early career researcher

An early career researcher is an interesting creature – focussed, driven and often self-critical. Outgoing Chair of the Early Career Committee (ECC) at NeuRA, Kirsten Coupland, explains what it is like being a young scientist and the role the committee plays in supporting careers.

Early career researchers are those working in science who have completed their PhD less than six years previously or who are under the age of 40; whether studying or employed, involved in academia, or industry. There are around 120 early career researchers currently at NeuRA but this number fluctuates as people take exciting steps in their careers. These researchers are just discovering what a career in research entails. They are finding that a scientific career is not as structured as one in the corporate world; skills are learnt on the job and successful outcomes to experiments often initially elude them. Young researchers learn at the deep end. The work of the ECC, of which I am the outgoing Chair, is important for young researchers at NeuRA. We provide events and seminars that develop the skills and professional attributes young researchers need to cultivate a successful career in science.

What it takes to be a scientist

The world of research is extremely competitive and many of the things that set one scientist apart from the crowd are less tangible than research results. Being a good scientist requires the ability to communicate, have a strong network, a comprehensive knowledge base and confidence.

KC_9453

Kirsten Coupland in the laboratory

What we do 

NeuRA’s ECC aims to give young researchers the ability to cultivate these assets and enjoy themselves at the same time. Events the ECC orchestrates encourage young researchers to interact with new people from different research groups. In doing so, they not only become confident at communicating their research to scientists from other fields, but they also start developing a network they will use throughout their career. Initiatives include regular seminars featuring speakers from around the country who discuss topics such as ethics, social media, and where to source funding.

Panel discussions of post-docs or non-academic science careers have helped get early career researchers thinking about what they will do with their scientific knowledge. Informal coffee meet-ups allow students to discuss their research with a mixed audience and interact with people they may not know at NeuRA. Early career researchers are the future generation of scientific research. It is important they have the skills and attributes necessary to carry out creative and exciting science that will revolutionise the way we understand the human body.    

Cannabidiol – a glimmer of hope for Alzheimer’s disease?

Alzheimer’s disease is the most common form of dementia, which affects around 330,000 Australians. In 2009 – 2010, the healthcare cost of dementia was over 4.9 billion dollars in Australia. Both of these figures are on the rise, given that our life expectancy is increasing.

People living with Alzheimer’s disease experience a range of symptoms that include social withdrawal and problems with remembering places, objects and people, and these symptoms become progressively worse with time. In the brain, aside from the increasingly well-recognised amyloid plaques and tangles, imaging and post-mortem analyses have also found extensive neuronal degeneration, inflammation, toxicity and oxidative stress, and these processes are likely to contribute to the development of Alzheimer’s disease.

Current treatments are unable to stop the disease progression, and the quest to find a viable treatment for Alzheimer’s disease continues. Many treatments have been designed to target single brain systems that are affected in Alzheimer’s disease. However, this approach is not sufficient for two reasons: 1) more than just one system is affected in the disease, and 2) it may be too late to administer these treatments once the disease has been diagnosed. Research now suggests it may be more beneficial for patients if treatments targeted a range of systems that are altered in Alzheimer’s disease and could be administered early, perhaps even before disease symptoms are prominent, as a method of prevention.

So where does one find a treatment that can exert neuroprotective, anti-oxidant and anti-inflammatory effects all at once? Well, the answer might lie in a compound known as cannabidiol. Cannabidiol has been shown to have all the above properties, which could be relevant for Alzheimer’s disease. However, there have been only a few studies that have followed up on this link, perhaps because many people might be eager to dismiss cannabidiol as a treatment due to concerns that it may exhibit the psychoactive properties of other compounds obtained from the cannabis plant. But in fact, cannabidiol is behaviourally inactive in humans when taken over long periods of time, including in people with schizophrenia and Huntington’s disease. Cannabidiol also prevents the memory-impairing effects of THC, the main psychoactive compound of cannabis. And, in promising news for Alzheimer’s research, cannabidiol has also been shown to reduce amyloid production and increase neurogenesis in brain cells. With this in mind, it is only logical that cannabidiol should be tested for its potential to benefit those with Alzheimer’s disease, as it might counter some of the main biological changes that are occurring.

David Cheng has just completed his PhD at NeuRA under the supervision of Dr Tim Karl.

David Cheng has just completed his PhD at NeuRA under the supervision of Dr Tim Karl.

My study, published in the journal Psychopharmacology, was the first to investigate the effect of cannabidiol treatment in a transgenic mouse model of Alzheimer’s disease. This mouse model carries two genetic mutations that are associated with familial Alzheimer’s disease, and the mice show behaviours that are relevant to Alzheimer’s symptoms, such as social recognition and spatial memory deficits. Since normal mice have a tendency to explore either new things or other mice, we compared how well transgenic mice fared in a test called the social preference test, which measures the amount of time that the test mouse spends exploring either a familiar or a new (never before seen) mouse. I discovered that the Alzheimer’s model mice spent the same amount of time exploring both the new and familiar mice, showing that they were unable to tell the difference between the two. Excitingly, daily cannabidiol treatment given over 3 weeks restored the social recognition memory of the transgenic mice.

In a separate study, soon to be published in the Journal of Alzheimer’s disease, cannabidiol was given to the transgenic mice every day, beginning at a very early age, to test whether it can be administered early as a prevention against the social recognition memory deficits. Promisingly, the development of recognition deficits in the disease model mice was prevented by the cannabidiol treatment. Using various biochemical techniques, I also found evidence to suggest that this effect might be mediated by the anti-inflammatory properties of cannabidiol.

These findings are extremely interesting as they show cannabidiol might have behavioural and biological effects that could benefit people with Alzheimer’s disease. Of course, we know that mice are not exactly like humans, but mouse models give researchers a great amount of insight into the effects of Alzheimer’s disease genetic mutations on both behaviour and biology. For example, links can be drawn between the social recognition deficits displayed by the Alzheimer’s disease model mice and the inability to recognise familiar faces in people with Alzheimer’s disease. Imagine what it would mean for people with Alzheimer’s disease and their friends and relatives if they could still recognise their loved ones! With more research, it will be possible to gain a better understanding of the exact mechanisms behind the beneficial effect that cannabidiol has already shown in this mouse model, paving the way for possible clinical trials in the future.

Building blocks for a fresh understanding of schizophrenia

Dr Dipesh Joshi received this year’s Leslie Kiloh paper award for his work into the understanding of schizophrenia. Since then, he has published new work linking problematic neurons to a genetic abnormality associated with schizophrenia.

He explains how his work has created a greater understanding of this disease…

Genes are a precious gift that every generation passes on to the following one since the existence of mankind. Abnormal functioning of some of these genes may lead to abnormal functioning of the brain cells leading to development of brain disorders. NRG1 and ErbB4 are two such genes that have been identified as ‘schizophrenia risk genes’.

Altered functioning or signaling of these genes contributes to the development of schizophrenia. Research shows that there are physical differences in the brains of people with schizophrenia compared with those of healthy people. To identify how genetic abnormalities lead to such physical differences remains a significant challenge. If this was known, we would be closer to understanding exactly what happens in the brain to cause the symptoms of schizophrenia, such as social withdrawal, difficulty with memory and planning, and even hallucinations, all of which can be very distressing to an individual with the illness.

What drug treatments are available now?

These days, the available antipsychotic treatments are relevant only for positive symptoms such as hearing voices, suspiciousness, feeling as though you are under constant surveillance, delusions, or making up words without a meaning, but not for negative symptoms which might include social withdrawal, cognitive deficits, difficulty in expressing emotion and an inability to feel pleasure. This highlights the urgency of having new antipsychotic drugs that have beneficial effects in treating negative symptoms and cognitive deficits in people with schizophrenia.

What are the risk genes doing in schizophrenia?

Dr Dipesh Joshi is a postdoctoral research officer at NeuRA

Dr Dipesh Joshi is a postdoctoral research officer at NeuRA

Our recent research work has been able to link schizophrenia risk genes (NRG1 and ErbB4) with a type of brain cell which maintains the inhibitory-excitatory balance in a normal brain. In schizophrenia, this particular brain cell-type, called inhibitory interneuron has been found to be reduced compared to healthy individuals. Research conducted in our laboratory is completely unique as it shows how an increase in the risk gene (ErbB4) is linked with a reduction in inhibitory brain cells. Increased levels of ErbB4 gene contributes to the inhibitory-excitatory imbalance resulting in development of schizophrenia.

These findings are crucial for brain researchers to understand how schizophrenia ‘risk genes’ adversely affect brain cells resulting in brain abnormalities found in people with schizophrenia. Our findings are a step forward in identifying new therapeutic targets for a new generation of antipsychotics that will have beneficial effects that extend beyond positive symptoms in people with schizophrenia and for us that is a very exciting prospect.

 

Are you a healthy control?

How about becoming a healthy volunteer for research and helping us Discover ~ Conquer ~ Cure? 

Do you have spare time and want to make a difference to people’s lives? Perhaps you’re willing to give up your time and participate in studies right here in Randwick?

I’m Connie Severino and my job at NeuRA is to maintain our healthy volunteer database that provides researchers with an easy way to recruit people for their studies.

We are always looking to recruit healthy volunteers because we want to make a difference to the lives of many who have suffered or are currently suffering neurological illnesses.

Healthy volunteers play an important part in supporting our research programs.

Each group within NeuRA covers a different area of research ranging from Alzheimer’s disease, chronic pain, falls and balance, Frontotemporal dementia, Parkinson’s disease, sleep apnoea, stroke, and many more. We recruit healthy volunteers for all of these areas.

We use data we collect from our healthy volunteers and compare it with the data we have from those affected with a particular neurological condition.

A healthy volunteer, often referred to as a ‘control’ or who sits within a ‘control group’, is simply a standard of comparison for checking or verifying the results of an experiment. Controls are the standard against which experimental observations are evaluated.

Becoming a volunteer does not cost you anything, however we do ask for your time and patience. Initially we ask you to complete a questionnaire and, from there, if you meet the control criteria, we register you on our Healthy Volunteer Registry that allows you to be selected up to three times a year.

What do I need to know? 

Often researchers will ask for clear specifications in controls such as age, gender, right or left handedness or walking ability. Once you are selected for a study, the researchers are notified and will contact you and ask you to participate.

Zeng copy

Jacqui Zheng with a volunteer for a falls and balance study at NeuRA

Each group’s tasks and activities vary but, rest assured, you will be well informed as to the specific tasks required of you before the trial begins. We endeavor to accommodate all your needs from travel arrangements, pick up and parking depending on your location and, at all times, keep you comfortable and informed.

We look for participants housed all over the country, particularly in NSW and the ACT. That said, due to most testing taking place here in Randwick, we typically invite volunteers from the Sydney metro and surrounding areas to join us, for ease of travel.

How do I get involved? 

Once you become a registered volunteer, you are not obliged to accept every invitation you are offered and you are of course free to withdraw from being on the registry at any given time.

Our registry has been active for approximately four years and has been beneficial for 30 studies to date. Some of our volunteers have returned to us multiple times as they enjoy the process and the ability to contribute to medical science in this way.

If you are interested in contributing your time, please see our website for further details or contact me directly on (02) 9399 1155. I am happy to answer any questions you might have.

It’s my belief that ‘A problem shared is a problem halved’… we thank all those who have helped in the past and who continue to volunteer.