Dementia and Parkinson’s disease are the two most common neurodegenerative diseases. And while dementia is the second leading cause of death in Australia with one new case every six minutes, and Parkinson’s disease affects 1 in every 340 (70,000) Australians, there is no treatment – only options to relieve symptoms.

Before they can find a cure, researchers need to better understand how neurodegenerative diseases develop.

Without a medical breakthrough, the number of Australians living with dementia is set to soar from 413,106 to 900,000 by 2050. Parkinson’s disease cases are also expected to double by 2030 as our population ages, currently costing the Australian economy more than $1.1 billion each year.

With your support, we can fund urgent research into Parkinson’s disease and dementia treatments.

Donate to Neurodegeneration Research Appeal now

or Parkinson's Appeal here.

Neurodegenerative Disease Research:

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Assoc Prof Lyndsey Collins-Praino

Senior Lecturer, Discipline of Anatomy and Pathology, University of Adelaide

The evolution of decision-making impairment in Parkinson’s disease: Prediction and prevention

University: Adelaide University

Funding: James & Diana Ramsay Foundation $73,229 x 3 years total $ 219,687

Project: This project will develop a comprehensive behavioural testing battery to characterise differences in the integrity of specific basal ganglia circuits involved in decision making in different subtypes of PD. Additionally, we will identify genes relevant to basal ganglia circuit function that may predict risk and progression of cognitive decline in PD.

“Cage fighting” for Parkinson’s Disease: How can we prevent the spread of abnormal proteins?

A major contributor to the spread of Parkinson’s disease throughout the brain is the transmission of an abnormally folded protein, called alpha synuclein, from brain cell to brain cell. The aim of this project is to pioneer a novel technology to target this alpha synuclein within the extracellular space and clear it from the brain. This may help to stop the brain transmission of alpha synuclein, halting the spread of the disease, and leading to a disease-modifying treatment strategy for PD.

Assoc Prof Lyndsey Collins-Praino

Senior Lecturer, Discipline of Anatomy and Pathology, University of Adelaide

The role of pericytes in delayed post-stroke neurodegeneration

Stroke is a leading cause of death, disability and dementia worldwide. However, loss of brain tissue distal to the primary stroke site, can occur months to years following stroke, increasing patient disability. This process is called secondary neurodegeneration and the underlying mechanisms of this delayed neuronal loss remain poorly understood. Pericytes are known to be involved in the early injury pathways following stroke; however, they may also contribute to delayed neurodegeneration given their roles in maintaining blood-brain barrier structure, transport, controlling blood flow, driving new cell growth and formation of new blood vessels. Despite this, no studies have investigated the contribution of pericyte changes to secondary neurodegeneration post-stroke. Accordingly, this study seeks to further understand what drives secondary neurodegeneration and whether pericytes are key contributors to post-stroke neurodegeneration. Specifically, we will examine the course of pericyte changes following stroke and determine alterations in key neurodegenerative and neuroinflammatory markers

Assoc Prof Lyndsey Collins-Praino

Senior Lecturer, Discipline of Anatomy and Pathology, University of Adelaide

Does TLR4 activation mediate the relationship between TBI and Parkinson's Disease

Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease, affecting 10 million people worldwide and 1 in every 350 Australians. While the exact causes of PD are currently unknown, one risk factor is traumatic brain injury. Despite growing awareness of the link between TBI and PD, however, brain mechanisms that account for this relationship are unknown. One potential mechanism may be neuroinflammation. A potent inducer of neuroinflammation is activation of Toll-like receptor 4 (TLR4), a pattern recognition receptor broadly expressed in the central nervous system. The current study will investigate whether the development of neuroinflammation and PD-like pathology following TBI is mediated by TLR4 activation. This has the potential to shed light on the mechanism by which a major risk factor for PD may lead to disease, and may help to identify novel therapeutic targets.

Assoc Prof Lyndsey Collins-Praino, previously investigated how brain inflammation changes over time, and whether this is associated with brain changes characteristic of neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease. One major risk factor for these diseases is traumatic brain injury (TBI). While it is not yet clear how TBI can lead to the brain changes seen in PD, often decades after the original injury, TBI is known to be associated with the induction of significant inflammation in the brain. This may set the stage for the later emergence of neurodegenerative disease. This raises the exciting possibility that targeting inflammation after injury may help to reduce the incidence of these conditions, at least in a subset of the population.

Assoc Prof Collins-Praino is also focused on understanding the brain mechanisms that underlie cognitive impairments, such as memory problems and difficulties with planning and paying attention, in these conditions.

Neurodegeneration Concussion Research:

The role of alcohol in promoting the development of neurodegeneration following a repeated concussion

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Dr Frances Corrigan

Senior Lecturer in Anatomy, School of Health Sciences, University of South Australia

A history of repeated concussions has been linked to three times higher risk of developing a neurodegenerative disease, to which there are currently no effective treatments. How repeated concussion promotes neurodegeneration, and what role alcohol abuse plays in that process, is poorly understood, making it difficult to intervene in the disease process. Work is ongoing to characterize the effects of chronic alcohol exposure on pathological changes following repeated concussion and determine whether this leads to long-term changes in behaviour, particularly cognition, depressive-like behaviour, and anxiety. This is particularly important given the accepted usage of alcohol within the community and the lack of understanding of what constitutes a safe level of alcohol consumption following a mild traumatic brain injury.

An especially common injury in contact sports such as football, chronic traumatic encephalopathy is a neurodegenerative disease, which appears to be exclusively related to repeated concussion.

Dr Francis Corrigan Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease which appears to be exclusively related to repeated concussion. This research considers the mechanisms by which systemic inflammation accelerates the disease process, leading to neuronal cell death.

Dr Francis Corrigan’s research examines how concussion – particularly repeated concussion – may increase the risk of developing cognitive deficits later in life. Previous research has suggested that levels of substance P (SP) are higher in adolescents and thus they may have a greater inflammatory response to a concussive insult than an adult. We will be investigating whether blockade of this inflammatory response – by preventing the actions of SP – will prevent the development of cognitive deficits following concussion in adolescence.

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