Traumatic Brain injury (TBI) is the leading cause of disability and death worldwide and is associated with significant impairment in brain function, impacting cognitive, emotional, behavioural and physical functioning. It is estimated that as many as 54-60 million people worldwide suffer from a TBI each year. While the acute effects of TBI are well characterized, a significant number of people affected by TBI develop long-lasting neuropsychiatric and cognitive impairments. TBI is also a significant risk factor for later development of dementia and Parkinson’s disease, although the brain mechanisms behind this association are still poorly understood.

Spinal Cord Injury (SCI) leaves patients disabled and dependent for basic daily activities. There are currently no effective treatments available for SCI and novel therapies are urgently required to reduce such devastating disability.

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Traumatic Brain Injury Research:

Identifying biomarkers to predict outcome following traumatic brain injury

Traumatic brain injury (TBI) encompasses pathophysiological changes known as secondary injury processes that often lead to worsened prognosis and outcome. To date there is no reliable methodology to predict which patients may deteriorate acutely following TBI. This project aims to investigate the immediate inflammatory response to TBI, via cerebral microdialysis, which allows direct sampling of the fluid within the brain to determine if alterations in the expression of any proteins within the inflammatory response predict the later development of brain swelling. The ability to identify these patients earlier, allows therapeutic intervention to begin which may prevent these deleterious outcomes.

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Ms Lola Kaukas PhD Student

University of South Australia

Characterising gut alterations following traumatic brain injury

Traumatic brain injury (TBI) is the leading cause of death in individuals under the age of 45 years and survivors are often left with long-term disability. In particular, patients with post-TBI gastrointestinal dysfunction have increased morbidity and longer periods of hospitalization. Therefore, treatment modalities targeting prevention of gastrointestinal dysfunction have important clinical implications. In the current study we will characterise both the time course and nature of gastrointestinal disturbances following trauma. As such, this study will evaluate the extent of gastrointestinal disturbances, including gut injury, increased permeability and alterations in inflammatory mediators, that occur following moderate traumatic brain injury. This may lead to the identification of novel therapeutic targets to reduce gastrointestinal complications and improve TBI patient quality of life.

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Assoc Prof Stuart Brierley

Mathew flinders Fellow in Gastrointestinal Neuroscience Flinders University

Developing TMS-EEG indices of functional and physiological deficit following mild traumatic brain injury

Mild traumatic brain injury (mTBI) is one of the most common forms of acquired brain injury, affecting millions of people around the world every year. Although once considered a short-lived injury, the potential long-term side effects of mTBI are now being increasingly recognised. Despite this, the physiological mechanisms contributing to these deficits are largely unknown, placing considerable limitations on how mTBIs are handled clinically. Using advanced neuroimaging techniques, my work aims to better understand how mTBI changes the brain, and how these changes result in ongoing functional deficits. This will allow us to develop markers of injury that can be used to track recovery from mTBI, and may eventually facilitate the design of interventions to reduce the burden of ongoing symptoms.

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Dr George Opie PhD

NHMRC Early Career Fellow, Discipline of Physiology, The 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.

While the acute effects of traumatic brain injury (TBI) are well-known, a number of individuals affected by TBI also develop chronic problems such as depression and cognitive impairment. Although the brain mechanisms of these impairments are currently unclear, persistent inflammation in the brain may play a key role.

Our current NRF-funded research projects investigate whether reducing brain inflammation immediately after injury can improve long-term outcomes in an experimental model of TBI. This work may have important consequences for the prevention of neurodegenerative diseases, such as dementia.

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Assoc Prof Lyndsey Collins-Praino

Lecturer in Anatomy & Pathology, Adelaide Medical School, The University of Adelaide

Spinal Cord Injury Research:

Investigating the relationship between neuroinflammation and the development of cognitive deficits following traumatic spinal cord injury: Can Fyn kinase inhibition break the link?

Spinal cord injury is commonly thought of as a disorder of paralysis, however, there is emerging evidence to suggest that an injury to the spinal cord can also affect the brain, initiating an inflammatory response resulting in cognitive deficits. Our research is focused on investigating the neuroinflammatory response within the brain following traumatic spinal cord injury and how this may lead to cognitive decline. Additionally, we are interested in how location may affect these results, specifically whether a higher (cervical) or lower (thoracic) injury causes greater cognitive decline. Our final aim is to determine whether inhibition of the neuroinflammatory response will improve cognition providing a potential treatment for SCI individuals against cognitive decline.

Dr Anna Leonard’ research is targeting raised pressure within the spinal cord after a traumatic spinal cord injury. Future studies will focus on increasing the space in which the spinal cord exists to accommodate for its increased volume due to swelling. This will alleviate the subsequent pressure increase, promoting tissue survival and reducing functional deficits.

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Dr Anna Leonard

Lecturer in Anatomy & Pathology, Adelaide Medical School, The University of Adelaide

Assoc Prof Lindsey Collins-Praino speaks further about her research.

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