Assoc Prof Lyndsey Collins-Praino, PhD image

Assoc Prof Lyndsey Collins-Praino, PhD

Senior Lecturer, Adelaide Medical School, University of Adelaide; Translational Neuropathology Laboratory, University of Adelaide: Traumatic Brain Injury Research and Parkinson's Disease Research

Current position:

  • Senior Lecturer, Adelaide Medical School, University of Adelaide
  • Head, Neurodegenerative Disease Research Group

Professional achievements:

  • SA Young Tall Poppy Award, 2016 (Finalist: SA Tall Poppy of the Year)
  • SA Early Career STEM Educator of the Year, Tertiary Education, 2016
  • Executive Dean’s Award for Teaching Excellence, 2015
  • Unsung Hero of South Australian Science, Finalist, 2015
  • Henry Taub Award, Taub Institute Faculty Retreat, Columbia University Medical Center, 2012
  • Outstanding Scientific Presentation, University of Connecticut Health Center Annual Neuroscience Retreat, 2010
  • Tieman Research Prize, NEURON conference, 2010


Parkinson’s Disease Research: Assoc Prof Collins-Praino’s research focuses primarily on understanding the brain basis of cognitive impairment in Parkinson’s disease. Almost 25% of Parkinson’s disease patients suffer from some degree of cognitive impairment at diagnosis, and, by 20 years after diagnosis, over 80% of individuals go on to develop Parkinson’s disease dementia (PD-D). PD-D is currently a major area of unmet clinical need, as it does not respond well to traditional drug therapies or neurosurgical techniques used to treat the motor symptoms of the disease. In fact, deep brain stimulation (DBS), the most common neurosurgical treatment strategy for Parkinson’s disease, may actually worsen cognitive function. Since PD-D is a major predictor of mortality and quality of life in individuals with Parkinson’s disease, the development of new treatment strategies is critical. Assoc Prof Collins-Praino’s research focuses on understanding changes in the brain that may lead to cognitive dysfunction in PD, particularly the role of neuroinflammation (inflammation in the brain) in this process, in order to identify novel treatment targets. Current projects in this area include:

  • Testing a drug that may suppress inflammation in the brain in order to treat both motor and non-motor symptoms of the disease, and protect dopamine neurons from death.
  • Studying people with Parkinson's disease and dementia with Lewy bodies in order to identify novel biomarkers that can predict the emergence and trajectory of cognitive dysfunction in the disease. Conducted in collaboration with Professor Masahisa Katsuno (Nagoya Graduate School of Medicine, Nagoya, Japan)
  • Investigating brain blood flow and its relation to cognitive function in Parkinson's disease. Conducted in collaboration with Dr Hannah Keage (School of Psychology, Social Work and Social Policy, University of South Australia).

A growing body of evidence suggests that traumatic brain injury is a significant risk factor for neurodegenerative disease, particularly dementia and Parkinson’s disease. The brain mechanism that links traumatic brain injury, even early in life, to the later emergence of these diseases is currently unknown. Assoc Prof Collins-Praino’s research focuses on investigating how neuroinflammation may drive this relationship.

Current NRF-funded projects include:

The role of pericytes in delayed post-stroke neurodegeneration (2019)

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.

“Cage fighting” for Parkinson’s Disease: How can we prevent the spread of abnormal proteins? (2019)

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.

Does TLR4 activation mediate the relationship between TBI and Parkinson’s Disease (2017 and 2018)

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

Developing imaging biomarkers that predict pre-frontal cortex deficits following concussive insults in adolescence (2017)

Traumatic brain injury (TBI) is common during childhood and adolescence, with most injuries classified as mild (concussions), but these can still have long-lasting consequences. Indeed, the paediatric population take longer to recover from concussive insults than adults and report higher rates of impulsivity, attention deficits and cognitive impairment post-injury. This longer recovery may relate to ongoing brain development in this population. In particular the pre-frontal cortex which continues to mature into early adulthood is important for the development of executive functions which control judgement, planning, impulsivity, and working memory. As such the age of onset of a concussion may interrupt the normal maturation processes within this region leading to ongoing impairment of executive functions. This project aims to investigate whether the age at which a concussive impact occurs can have differential effects on the development of the pre-frontal cortex. This will be through examination of effects on executive function in adulthood- by examining impulsivity, working memory and judgement and linking this to changes in the key neurotransmitter systems within this region of the brain. Importantly this will be linked to magnetic resonance imaging (MRI) measures that will identify whether there are any signature alterations that can be linked to persistent behavioural changes.

Does norepinephrine mediate the relationship between inflammation and chronic cognitive and neuropsychiatric impairments following Traumatic Brain Injury? (2016)

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. This inflammation may be driven by reductions in the neurotransmitter norepinephrine. Our research will investigate whether increasing levels of norepinephrine immediately after injury can reduce brain inflammation and prevent the development of persistent deficits in an experimental model of TBI.

Ability of Granulocyte Colony Stimulating Factor to Improve Long-Term Cognitive Consequences Following Traumatic Brain Injury (2015)

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. TBI is also a significant risk factor for later development of dementia and Alzheimer’s disease. This research uses an experimental model of TBI to investigate how markers of neuroinflammation and neurodegeneration are related to cognitive impairment up to one year post-injury. The model is also used to investigate whether treatment can reduce neurodegeneration and improve cognition. Understanding TBI is a critical first step in developing novel treatment strategies for long-term complications of TBI.

Personal Reflection:

Why neurosurgery / neurosurgical research?

  • When I began work in a neuroscience research lab, I fell in love with research and knew instantly that I wanted to head my own research lab, so I decided to pursue a PhD in neuroscience and an academic career.

Please share any special moment you can think of which reinforced to you that neurosurgery and or neurosurgical research was the career for you.

  • I have been fortunate to volunteer as a speaker to support groups for those with Parkinson’s disease and their caregivers. The opportunity to meet with these individuals has been invaluable, and has helped to place my research in perspective. It helps me to remember why this work is important, and how many people it has the potential to help.

Neuroscience, neurology and neurosurgery are tough, but rewarding, careers. There will be days when you wonder why you chose to pursue such a challenging field, or when you feel frustrated by limitations in current treatment options for these debilitating neurological conditions. In spite of this, never lose sight of the ultimate goal: to improve life for the millions affected by these conditions. I’m always reminded of the Jane Goodall quote, “What you do makes a difference, and you have to decide what kind of difference you want to make.” What we do in this field does, indeed, make a difference. It’s important not to forget that.


For a full list of Assoc Prof Collins-Praino's publications, please visit her Google Scholar page.

Collins-Praino L, Corrigan F (2017). Does neuroinflammation drive the relationship between tau hyperphosphorylation and dementia development following traumatic brain injury? Brain, Behaviour, and Immunity, 60. 369-382.

Spinelli J, Collins-Praino L, Van Den Heuvel C, Byard R (2016). Evolution and significance of the triple risk model in sudden infant death syndrome. Journal of Paediatrics and Child Health.

Corrigan F, Arulsamy A, Teng J, Collins-Praino L (2016). Pumping the Brakes: Neurotrophic Factors for the Prevention of Cognitive Impairment and Dementia after Traumatic Brain Injury. Journal of Neurotrauma. 34(5), 971-986.

Collins-Praino, L.E., Francis, Y., Griffith, E., Weigman, A., Urbach, J.A., Lawton, A., Honig, L.S., Cortes, E., Vonsattel, J.P.G., Canoll, P., Goldman, J.E. and Brickman, A.M. (2014). Soluble amyloid beta levels are elevated in the white matter of Alzheimer’s patients, independent of cortical plaque burden. Acta Neuropathologica Communications. doi: 10.1186/s40478-014-0083-0.

Collins-Praino, L.E., Paul N.E., Ledgard F., Podurgiel S., Kovner R., Rhodes C., Hussain N., Baqi Y., Muller, C.E., Senatus P.B. & Salamone J.D. (2013). Deep brain stimulation of the subthalamic nucleus effectively reverses tremulous jaw movements induced by both dopamine antagonism and cholinergic stimulation in a rodent model of parkinsonian tremor: Interaction with the effects of adenosine A2A antagonism. European Journal of Neuroscience, 38(1), 2183-2191.

Collins, L.E., Paul, N.E., Abbas S.F., Leser C.E., Podurgiel, S.J., Galtieri, D.J., Chrobak, J.J., Baqi, Y., Muller, C.E. & Salamone J.D. (2011). Oral tremor induced by galantamine in rats: A model of the parkinsonian side effects of cholinomimetics used to treat Alzheimer’s disease. Pharmacology, Biochemistry, and Behavior, 99(3), 414-422.

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