Our researchers

Psychotropic medications, i.e., medications that can act on the brain, are often used to treat changed behaviours related to dementia. Inappropriate use (where the actual or potential harms of therapy outweighs the benefit for the individual) of psychotropic medications is particularly high among older adults living with dementia in residential aged care facilities. The usage rates vary among residential aged care facilities, and the organisational culture is an important contributor. This proposal aims to validate an organisational culture evaluation tool so that residential aged care facilities providers can identify the tailored strategies needed to support the appropriate use of psychotropic medications in residents living with dementia. We will be partnering with aged care stakeholders, including people living with dementia and their carers to provide feedback on the tool. We will also recruit residential aged care facilitystaff and healthcare professionals to participate in a survey to ensure that items in the tool measure what it is intended to measure and enable scoring of the tool to provide feedback to residential aged care facilitiy providers. The research project will provide a validated, user-friendly tool to evaluate residential aged care facility organisational culture to support the appropriate use of psychotropic medications in people living with dementia.

Changes in behaviours such as aggression, apathy and depression are common in dementia and contribute to more problems with doing everyday activities, more rapid memory loss, and more reliance on carers/family. They are often reported as a reason for entry into aged care. New research has shown that later-life behavioural changes before the onset of memory problems, known as Mild Behavioural Impairment (MBI), are an early warning sign for dementia. Research is now needed that will help us understand why some people are more vulnerable to MBI while others are resilient, how early detection of this dementia-risk marker can be used to help health care professionals and families manage the clinical presentation of MBI, how care service provision can be supported, and relationships safeguarded. A better understanding will help inform clinical diagnostics and care provision strategies. My research program provides the world-first opportunity to answer these important questions. I will do this by drawing on 20 years of data from the PATH Through Life Project and by leading the first Australian Survey of Knowledge and Understanding of MBI (ASKU-MBI). This understanding is urgently needed to improve early diagnosis and treatment of this dementia-risk marker in Australia.

The availability and accessibility of post-diagnostic support for people living with dementia and carers is of central importance in dementia care. People with dementia and their carers require access to timely education, emotional and practical support, lifestyle advice, and meaningful activities, to maximise their quality of life and to potentially delay cognitive decline. Allied health professionals at Canberra Health Services at the University of Canberra Rehabilitation Hospital and the University of Canberra have designed an evidence-based 12-week multicomponent program, tailored to people with dementia and carers, which includes physical activity, social engagement, nutrition assessment, education, and capacity building. The team engaged with Dementia Australia advocates to refine the program and set priorities for research. The research project will assess the value of the multicomponent dementia support program, perform a pilot study to measure impact and effectiveness, and explore barriers to access to post-diagnostic dementia support services for people with dementia and carers. The project has the potential to become part of standard care in the ACT region, and to set an example for dementia care services Australia-wide.

A personalised cognitive strategy program delivered by an Amazon Alexa Echo Show 8 (Alexa) using natural conversations may be more acceptable than some of the traditional digital health approaches such as internet browsers, tablets and smart phones. Alexas present an ideal method to deliver personalised strategies such as medication/appointment reminders or assist people with mild cognitive impairment (MCI) and dementia to carry out activities of daily living such as meal preparation, as they can be automated to provide voice reminders and instructions which can prompt users to carry out scheduled activities throughout the day, and enable regular feedback to the prescribing health professional. We will conduct a co-designed 12-week trial of a home-based personalised rehabilitative strategy program delivered via an Alexa in older adults aged 60 years and older with MCI and/or dementia. We anticipate that a 12-week Alexa delivered home-based personalised rehabilitative strategy program will be feasible, acceptable and improve depression, cognition and activities of daily living compared to a control group. Data from this project will explore the delivery of this project to reduce healthcare inequalities in people with dementia by providing high quality and cost-effective services to underserved populations, such as low-income individuals and people in remote and rural areas.

The cause of Alzheimer’s disease (AD) is unclear, and there is a significant need for better treatment of the disorder. Inflammation in the brain i.e. neuroinflammation, is an established hallmark of AD, but it is unclear precisely how neuroinflammation interacts with and/or exacerbates other types of AD pathology. We hypothesise that neuroinflammation exacerbates other types of AD pathology. This hypothesis has not been investigated before, and we hypothesise that these complex interactions may present a new treatment avenue. We will test this hypothesis using a novel mouse model which combines neuroinflammation with AD pathology. We will also examine a novel treatment for neuroinflammation, AD pathology and cognitive impairment in a mouse model. Our research will determine if interactions between neuroinflammation and AD pathology are a critical component of AD aetiology, and if these interactions could be a new treatment target. 

Changed behaviours (e.g., aggression, socially-inappropriate behaviours) commonly occur in younger-onset dementia which typically affects people below the age of 65 years. These changed behaviours can have significant negative impacts on the person with dementia and their families such as reduced quality of life and increased stress for family carers. Medication is currently the most common intervention, though is often ineffective and causes side effects. Although behaviour support interventions, such as Positive Behaviour Support (PBS) are most effective, there is a serious lack of options for these in Australia.

Through five weekly education sessions, questionnaires and interviews, we will examine how acceptable and useful a family-directed PBS education program is in equipping family carers with more effective behaviour support. Our project will equip carers with the relevant skills to manage changed behaviours on a day-to-day basis, and thus reduce the negative impacts of changed behaviours. We will also examine the effectiveness of online delivery and develop facilitator guidelines to increase our ability to reach families supporting a person with dementia across Australia, particularly in regions with limited services. Our findings will improve dementia care in the community and the services available for families supporting a person with dementia with changed behaviours.

Dementia is the leading cause of disability in persons over the age of 65 in Australia, with Alzheimer’s disease alone accounting for more than 40% of all dementia cases. By addressing risk factors for developing dementia including hypertension, depression, and physical inactivity, one-third of Alzheimer’s Disease cases and up to 40% of all dementia cases may be preventable. Sleep disturbances including poor sleep quality, and shorter sleep duration, as well as sleep disorders such as sleep apnoea are present in up to 60% of older adults over the age of 60, and in up to 70% of those with dementia. These types of sleep problems are emerging as another significant yet modifiable (e.g. treatment with melatonin or CPAP devices) risk factor for dementia. However, to date how these sleep problems relate over time to brain and cognition changes, underlying dementia processes, and other risk factors has not been thoroughly investigated. We will address this gap through comprehensively characterising sleep problems in older adults with early dementia or at risk for dementia. Furthermore, we will develop tools that will provide personalised risk profile reports that can be implemented by clinicians to guide strategies for dementia management and prevention for individual patients.

Alzheimer’s disease is the most common form of dementia and neither an effective treatment nor a cure are currently known. This is partly due to a gap in knowledge on how brain cells deteriorate in Alzheimer’s disease. The last decades of research have established that amyloid and tau, two factors that are common in Alzheimer’s, work together in damaging brain cells. Whether there are protective factors that reduce this damage remained largely unknown. Recently, we have found a protective signal that targets tau and reduces damage to brain cells and memory.

This project aims to understand how this protective signal works in detail, how it helps maintain healthy brain function, and how it can be boosted to prevent memory loss associated with Alzheimer’s disease. This study employs latest technologies in assessing brain molecules and their function, brain activity, and strength of memory performance. As a result, we will better understand how protective factors in the brain are connected and how they can be activated and harnessed to reduce brain damage and memory loss in Alzheimer’s disease.

Many people with dementia eventually move into residential care. Making this decision and coping with admission processes can be stressful and distressing. These feelings may be heightened by the COVID-19 pandemic if families are not able to visit care facilities due to lockdown and/or are concerned about transmission. However, carers report that formal supports to help families cope during this time are lacking. This study aims to test delivery of a telephone/video counselling intervention during the residential care placement process to help reduce stress and distress for family carers. The Residential Care Transition Module (RCTM) consists of six telephone or video-link counselling sessions delivered to family carers over 12 weeks by a trained health or social care professional. It includes education about dementia and residential care facilities, dementia-specific grief counselling, stress reduction techniques, and referral to support networks. The proposed pilot study will test whether delivery of the RCTM following Aged Care Assessment Team approval for residential care is feasible and potentially beneficial in reducing family carer stress, anxiety, depression, guilt, and grief, and improving social support during the course of placement. This may help carers to better cope and adjust once their relative has been admitted into residential care.

Early pathogenic events in Alzheimer’s disease (AD) include a progressive loss in brain’s capacity to generate new neurons (i.e. neurogenesis) in the area important for learning and memory and degeneration of cells that produce a neurochemical, acetylcholine that is vital for cognitive functions. However, whether and how these two processes are linked remains an open question. In this project, we will investigate a direct link between these two cellular processes and cognitive functions and explore whether these deficits can be rescued by stimulating a select receptor that we have identified boosts the production of new neurons. Using a multi-modal approach involving animal models to monitor and manipulate specific neuronal populations, together with assessing cognitive functions, our research will provide the experimental evidence establishing the role of cholinergic neurons and a select cholinergic receptor in regulating adult neurogenesis and neurogenesis-dependent cognitive functions. The outcomes of this study may provide the mechanistic basis for the development of a new approach harnessing therapeutic potential of brain’s endogenous neuroplasticity mechanism to delay the onset or slow the progression of dementia.

Alzheimer’s disease and Frontotemporal Dementia are two of the most common causes of dementia. Unfortunately, there is currently no effective treatment or cure for either of these disorders. Therefore, the development and testing of new therapies is urgently required. Although these two dementias are quite distinct from one another, in both conditions, a protein known as Tau is thought to play a central role in the disease process. One mechanism by which Tau is thought to be involved, is via excessive interactions with another protein known as Fyn. Together, Fyn and Tau set off a cascade of events that lead to overstimulation of neuronal brain cells, eventually causing cell death. My work postulates that if interactions between Tau and Fyn could be disrupted or reduced in the brains of dementia patients, this would provide therapeutic benefits. Therefore, my research project aims to identify compounds that can disrupt interactions between Tau and Fyn by utilising a cutting-edge technology that can screen up to 14 billion compounds at once. Identified hits will then be tested in cell culture models to determine their potential usefulness. This will lay the groundwork for pre-clinical testing and, hopefully in the future, clinical trial testing in patients

Caring for a family member of friend living with dementia is often portrayed negatively, focusing on depression, burden and chronic stress. While there are negative physical and mental health impacts associated with caring, this is not the full picture. This study will develop a resource that aims to provide a more balanced view of the experience of caring. We will ask carers to share their stories of positive and negative aspects of caring. We will also ask them about the creative ways they manage daily stressors and challenges. The resource may be an animation or other audio-visual medium that will be widely accessible. We will use carers’ voices for authenticity and digital systems to measure how often the resource is viewed. The output will be suitable for the general public and go some way towards countering overly negative portrayals of caring for someone living with dementia.

The experience of anxiety and depression can lead to poor mental health and wellbeing. Good measures of these experiences are therefore important to help find out if someone has this type of diagnosis. Unfortunately, measures of anxiety and depression in Aboriginal and Torres Strait Islander (ATSI) populations are limited. This project therefore aims to develop measures of anxiety and depression that will be culturally appropriate, and therefore meaningful, within ATSI populations. To do this, we will hold yarning circles with members of the ATSI population to find out how they define anxiety and depression. We will then use experts in the field to help develop those discussions into a list of questions suitable for a questionnaire. This list will then be given to members of the ATSI population to see what they think and to see how useful the questionnaires are when used with people with anxiety and/or depression. We hope to create measures of depression and anxiety that will do a better job of identifying these diagnoses in members of the ATSI population. Being able to correctly identify these diagnoses will assist in better managing such conditions and in improving the overall wellbeing of members of the ATSI population.

Obstructive sleep apnea is a severe sleep disorder that can lead to a repeated lack of oxygen (intermittent hypoxia) in the brain during sleep. Studies have found that patients with this condition also have an increased risk of developing dementia (Alzheimer's disease). To study this link between sleep apnea and dementia, we have created a mouse model, which has the sleep disorder and develops dementia due to the repeated lack of oxygen in the brain during sleep. We have previously shown that this repeated lack of oxygen causes the loss of a specific type of brain cell (cholinergic basal forebrain neurons). The aims of this study are therefore 1) to test if treating these mice with existing drugs will prevent brain cell death and protect them from dementia and 2) to understand the specific mechanism of how lack of oxygen leads to brain cell death. Overall this project will lead to knowledge about the molecules involved in causing and preventing brain cell death as a consequence of repeated lack of oxygen. This knowledge is necessary for the development of prophylactic drugs that protect the brain and reduce the risk of dementia in obstructive sleep apnea patients.

Neglect and abuse of people living with dementia is a systemic problem in residential aged care. It inflicts significant harm on victims/survivors, care partners/families/friends and the broader dementia community. Those affected have been unable to access justice, or healing and closure through the courts. While stopping future neglect and abuse requires reform of legal, regulatory, and funding frameworks, these reforms do not ‘redress’ in the sense of setting right or fixing the wrongs of past neglect and abuse. Redress practices beyond individual court action (e.g. compensation and psychosocial support, memorials, national apologies, community education) create individual and community benefit by delivering financial, legal and community recognition of experiences through appropriate exposure and analysis of past wrongdoing. It is vital redress is considered by the Disability Royal Commission moving forward. This action research project will explore the need for redress through interviews and focus groups with people living with dementia, care partners/families/close friends and lawyers/advocates. Recommendations will be shared with the Disability Royal Commission, dementia community, government, aged care sector, advocacy organisations and professional associations. Anticipated benefits include a redress framework that can facilitate justice, healing and enhanced wellbeing for victim/survivors and the dementia community, and education and advancement of protections within future aged care and legal systems.

Poor eyesight makes living with dementia harder. Regular eye tests are vital to detect and treat poor eyesight. If not adapted to accommodate their needs, eye tests can be challenging or distressing for people with dementia, and caregivers supporting them. Our research aims to improve the experience of receiving eyecare (having an eye test and following eyecare advice), for people with dementia and family caregivers supporting them. Having good eyesight helps people with dementia maintain their independence, and live at home for longer. We will speak with people with dementia, family caregivers (both supported by a skilled interviewer) and eyecare professionals. This captures views of receiving, supporting and delivering an eye test.  The research lasts two years. 60 people will take part, including 20 people with dementia.  People with dementia and caregivers will guide our research, ensuring information we provide and questions we ask are relevant and clear. We will share our findings with them, to identify key messages informing:

• Information cards about dementia-friendly eye tests and eyecare, for people with dementia and caregivers, available at dementia cafes and day centres.

• Training for eyecare professionals, about delivering dementia-friendly eyecare. This makes it easier to seek and receive dementia-friendly eyecare.

Dementia and self-harm represent substantial public health burdens in the older population. Dementia has been identified as a risk factor for self-harm behaviour, particularly in older males. Research is needed to understand factors associated with self-harm in people with dementia to develop appropriate suicide and self-harm prevention programs. As people age, physical and mental health conditions along with social circumstances contribute to self-harm. Although contact with health services in the months before self-harm is common, little is known about these healthcare pathways that might inform prevention strategies. The growing ageing population, along with the high occurrence of dementia and self-harm in older adults, has substantial implications for the planning and equipping of health services to meet the needs of affected individuals.

Our study will use linked health data from NSW to understand the health problems and social circumstances of people with dementia who self-harmed and how they have accessed health services before and after self-harm. Understanding the specific health problems and treatment gaps is a critical first step to developing effective preventive measures. This will inform strategies to allow health services to better meet the needs of people with dementia who self-harmed.

The major hallmark of Fronto-temporal dementia (FTD) is the presence of protein clumps or ‘aggregates’ in affected neurons. These are present in various parts of the cell, including the nucleus, which acts as the cellular ‘brain’. Importantly, it is becoming apparent that the nucleus is an important site from where disease is initiated. However, due to the limited availability of appropriate tools, the role of protein aggregates in the nucleus and how this relates to FTD has not been previously studied. This project, using advanced tools and cellular techniques, aims to take an innovative approach to identify how these nuclear aggregates form in affected neurons in FTD. Furthermore, it aims to identify new ways to prevent the formation of these aggregates. We have found that a specific protein prevents the clumping of proteins in the nucleus. It is also protective against several other pathological events linked to FTD. However, similarly, this protein has not been previously studied in FTD. This project will therefore investigate a new cellular pathway in FTD and novel mechanisms to prevent the formation of aggregates. This study may therefore reveal novel therapeutic targets for FTD.

People living with cognitive impairments often experience loneliness and depression. They find it hard not just to remember things, but also talking to others. One person living with dementia said to me: “I worry that other people will laugh at me and say I don’t say things that make sense or I repeat myself. Many older adults with cognitive impairment have difficulties with recognising emotions and reacting in a socially appropriate way. Most treatments developed for dementia focus on improving memory and language. So far, there is no treatment that helps people recover or maintain social skills as their cognitive abilities decline. We want to change that. We will run focus groups with people living with cognitive impairments and their care partners. Together we will write a social skills training manual specifically designed for older adults with cognitive impairments. We will then run a pilot study to test the effectiveness of the social skills training. Our hope is that people living with cognitive impairments can reconnect with others and experience the joy of socialising once again.

Fronto-temporal dementia (FTD) is associated with progressive damage to the aspects of the human brain involved in the control of movement, problem solving, memory, social behaviour and other vital functions. Post-mortem sampling of the brains of people who have lived with FTD revealed the presence of large clumps of proteins, which are toxic and damaging to the brain. Researchers are yet to identify why these proteins begin to cluster. My research therefore aims to elucidate why and how these proteins clump. Further, the nerves of the brain have intrinsic protective waste-disposal mechanisms that are normally responsible for clearing up these protein clumps. However, in FTD these protective mechanisms fail. My research will potentially identify where the protein clumping begins, how the clumps overwhelm the brain’s waste disposal-recycle machinery for damaged proteins and help identify potential drugs that can halt or reverse the clumping of these proteins. My work has the unique potential of providing an early diagnostic tool prior to the observation of any FTD associated symptoms. Further, it will provide the opportunity to screen the effect of new drugs on the protein clumps prior to commencing clinical trials.