Assoc Prof Renée Turner, PhD image

Assoc Prof Renée Turner, PhD

Senior Lecturer, The University of Adelaide, NRF Director of Neurosurgical Research

Current positions:

  • NRF Director of Neurosurgical Research
  • Associate Professor and Deputy Head of Discipline, University of Adelaide
  • Head, Translational Neuropathology Laboratory


  • 2015 South Australian Young Tall Poppy Science Award (Australian Institute of Policy and Science)
  • 2014 Australian Society for Medical Research (ASMR) Leading Light Award - Runner up
  • 2008 NHMRC CJ Martin Overseas Biomedical Post-Doctoral Fellowship
  • 2006 Fresh Science, Finalist - Australia's Best Young Scientists
  • 2004 NHMRC Dora Lush Post-Graduate Fellowship

Research area:

Turner pursued a B.Sc. Honours Degree in 2002 with a focus traumatic brain injury, working with Corinna Van Den Heuvel and Robert Vink. This took a slight turn in 2004 when beginning her PhD, with her research now being focused on ischaemic stroke under the supervision of Robert Vink and Peter Blumbergs. It must be noted that while Turner studied in the laboratory at the time Robert Vink was the Chair of Neurosurgery, she was not an official Chair student and was not supported by the NRF.

Why neurosurgical research?

Turner explains: "As a student starting University I never imagined that I would be a neuroscientist developing treatments for neurological conditions such as stroke and traumatic brain injury. After my Science degree I pursued Honours and this was when I was introduced to research in my studies on traumatic brain injury. That was it, I was hooked. I made the decision then and there that neurosurgical research was what I wanted o pursue as a career. I feel very lucky that I am able to spend my working days asking research questions, trying to find out more information about how certain neurological conditions develop and progress, and most importantly, seek to develop new treatments to improve outcomes and survival. Now, I can’t imagine doing anything else as a career."

Current NRF-funded projects include:

Characterising gut alterations following traumatic brain injury (2019)

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.

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

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.

Pre-clinical Evaluation of New Stroke Treatments (2015)

Most strokes are caused by a blood clot lodging in an artery, blocking blood flow to the brain. The aim of treatment is to restore blood flow as soon as possible, minimising brain tissue death. A new preclinical model has been developed in the Neurological Diseases Laboratory which seeks to replicate this situation, allowing close study of how tissue injury and death occurs during stroke and of events that occur within the brain as blood flow is restored. This model will be used to study how damage may be minimised, working towards improved treatment and better outcomes for stroke patients.

Effects of NK1 antagonists on ICP and brain oxygenation after ovine stroke (2011)

Our laboratory has recently shown that NK1 tachykinin receptor antagonists are highly efficacious in reducing brain swelling, mortality and functional deficits in a rodent model of stroke (Turner et al., 2011). However, validation in a large animal model is an essential step towards clinical testing. We have recently developed a sheep model of middle cerebral artery stroke, which is the most common site of human stroke. This innovative and original model produces neuropathological and physiological changes similar to that observed in the clinical condition. This model also provides a sound platform for screening potential therapeutic agents for the treatment of stroke. We strongly believe that this approach will assist in the development of therapeutic agents and improve the likelihood of successful translation from basic science discoveries to clinical stroke treatment.

The aim of this proposal is therefore to characterise the potential of our novel pharmacotherapy (NK1 tachykinin receptor antagonists) as a therapeutic agent to reduce brain swelling and improve outcome in an ovine model of stroke that closely replicates human stroke. The proposal will involve inducing a 2 h reversible stroke in the adult sheep, and monitoring ICP and brain oxygenation over the following 24 h. Animals will be treated at 6 h with either the NK1 receptor antagonist, or with equal volume saline. The sheep model of stroke has ethics approval from the University of Adelaide and SAPathology.


For a full list of Associate Professor Turner's publications, please visit her Google Scholar page.

Busingye DS, Turner RJ, Vink R (2016). Combined Magnesium/Polyethylene Glycol Facilitates the Neuroprotective Effects of Magnesium in Traumatic Brain Injury at a Reduced Magnesium Dose. CNS Neuroscience & Therapeutics 22 (10), 854-859

McAteer KM, Corrigan F, Thornton E, Turner RJ, Vink R (2016). Short and Long Term Behavioural and Pathological Changes in a Novel Rodent Model of Repetitive Mild Traumatic Brain Injury, PLoS One 11 (8).

Leonard AV, Turner RJ (2016). Aquaporins within the Central Nervous System: Implications for Oedema Following Traumatic CNS Injury. Aquaporins in Health and Disease: New Molecular Targets for Drug Discovery, 205-215.

Turner RJ, Sharp FR (2016). Implications of MMP9 for blood brain barrier disruption and hemorrhagic transformation following ischaemic stroke. Frontiers in Cellular Neuroscience 10.

Wells AJ, Vink R, Helps SC, Knox SJ, Blumbergs PC, Turner RJ (2015). Elevated intracranial pressure and cerebral edema following permanent MCA occlusion in an ovine model. PLoS one 10 (6).

Turner R, Vink R (2014). NK1 Tachykinin receptor treatment is superior to capsaicin pre-treatment in improving functional outcome following acute ischaemic stroke. Neuropeptides 48 (5) 267-272.

Anderson RWG, Sandoz B, Dutschke JK, Finnie JW, Turner RJ, Blumbergs PC, Manavis J, Vink R (2014). Biomechanical studies in an ovine model of non-accidental head injury. Journal of Biomechanics 47(11) 2578-2583.

Gabrielian, L., Helps, S.C., Thornton, E., Turner, R.J., Leonard, A.V., Vink, R. (2013) Substance P antagonists as a novel intervention for brain edema and raised intracranial pressure. Acta Neurochir (Suppl), 118:201-4.

Lewis, K.M., Turner, R.J., Vink, R. (2013) Blocking neurogenic inflammation for the treatment of acute disorders of the central nervous system. Int. J. Inflammation, 578480.

Turner, R.J., Vink, R. (2013) The role of substance P in ischaemic brain injury. Brain Sci, 3: 123-142.

Wells, A.J., Vink, R., Blumbergs, P.C., Brophy, B.P., Knox, S., Helps, S., Turner, R.J. (2012) A surgical model of permanent and transient middle cerebral artery stroke in the sheep. PLoS ONE, 7: e42157.

Turner, R.J., Vink, R. (2012) Combined tissue plasminogen activator and an NK1 tachykinin receptor antagonist: an effective treatment for reperfusion injury following acute ischemic stroke in rats. Neuroscience, 220: 1-10.

Turner, R.J., Vink, R. (2012) Magnesium in traumatic brain injury, in Magnesium in Health and Disease (Eds. Watson R, Zibadi, S, Preedy, V) Springer, New York, p255-267.

Turner, R.J., Corrigan, F., Vink, R. (2012) Magnesium in acute brain injury, in Metal Ions in Stroke (Eds. Li, Y, Zhang J) Springer, New York, p 445-460.

Barry, C., Corrigan, F., Turner, R.J., Vink, R. (2012) New therapeutic approaches to subarachnoid hemorrhage. Expert Opinion on Investigational Drugs, 21:845-59.

Tian, Y., Stamova, B., Jickling, G.C., Xu, H., Liu, D., Ander, B.P., Bushnell, C., Zhan, X., Turner, R.J., Davis, R.R., Verro, P., Pevec, W.C., Hedayati, N., Dawson, D.L., Khoury, J., Jauch, E.C., Pancioli, A., Broderick, J.P., Sharp, F.R. (2012) Y Chromosome gene expression in the blood of male patients with ischemic stroke compared with male controls. Gender Medicine, 9:68-75e3.

Finnie, J.W., Blumbergs, P.C., Manavis, J., Turner, R.J., Helps, S.C., Vink, R., Chidlow, G., Dutschke, J., Anderson, R.W.G. (2012) Neuropathological changes in a lamb model of non-accidental head injury (the shaken baby syndrome). Journal of Clinical Neuroscience, 19(8): 1159-64.

Turner, R.J., Helps. S.C., Thornton, E., Vink, R. (2011) A substance P antagonist improves outcome when administered 4 h after onset of ischaemic stroke. Brain Research, 1393:84-90.

Zhan, X., Jickling, G.C., Tian, Y., Stamova, B., Xu, H., Ander, B.P., Turner, R.J., Mesias, M., Verro, P., Bushnell, C., Johnston, S.C., Sharp, F.R. (2011) Transient ischemic attacks characterized by RNA profiles in blood. Neurology, 77:1718-24.

Turner, R.J., Jickling, G.C., Sharp, F.R. (2011). Are underlying assumptions of current animal models of human stroke correct: From STAIRs to high hurdles? Translational Stroke Research, 2:138-143.

Turner, R.J., Bushnell, C.D., Register, T.C., Sharp, F.R. (2011) Gender-dependent correlations of carotid intima-media thickness with gene expression in blood. Translational Stroke Research, 2:171-178.

Jickling, G.C., Xu, H., Stamova, B., Ander, B.P., Zhan, X., Tian, Y., Liu, D., Turner, R.J., Mesias, M., Verro, P., Khoury, J., Jauch, E.C., Pancioli, A., Broderick, J.P., Sharp, F.R. (2010) Signatures of cardioembolic and large-vessel ischemic stroke. Annals of Neurology, 68: 681-92.

Jickling, G.C., Zhan, X., Ander, B.P., Turner, R.J., Stamova, B., Xu, H., Tian, Y., Liu, D., Davis, R.R., Lapchak, P.A., Sharp, F.R. (2010) Genome response to tissue plasminogen activator in experimental ischemic stroke. BMC Genomics, 11: 254.

Liu, D.Z., Tian, Y., Ander, B.P., Xu, H., Stamova, B.S., Zhan, X., Turner, R.J., Jickling, G., Sharp, F.R. (2010) Brain and blood microRNA expression profiling of ischemic stroke, intracerebral hemorrhage, and kainate seizures. Journal of Cerebral Blood Flow and Metabolism, 30:92-101.

Zhan, X., Ander, B.P., Jickling, G., Turner, R., Stamova, B., Xu, H., Liu, D., Davis, R.R., Sharp, F.R. (2010) Brief focal cerebral ischemia that simulates transient ischemic attacks in humans regulates gene expression in rat peripheral blood. Journal of Cerebral Blood Flow and Metabolism, 30:110-8.

Xu, H., Stamova, B., Jickling, G., Tian, Y., Zhan, X., Ander, B.P., Liu, D., Turner, R., Rosand, J., Goldstein, L.B., Furie, K.L., Verro, P., Johnston, S.C., Sgarp, F.R., Decarli, C.S. (2010) Distinctive RNA expression profiles in blood associated with white matter hyperintensities in brain. Stroke, 41:2744-9.

Stamova, B., Xu, H., Jickling, G., Bushnell, C., Tian, Y., Ander, B.P., Zhan, X., Liu, D., Turner, R., Adamczyk, P., Khoury, J.C., Pancioli, A., Jauch, E., Broderick, J.P., Sharp, F.R. (2010) Gene expression profiling of blood for the prediction of ischemic stroke. Stroke, 41:2171-77.

Stamova, B.S., Apperson, M., Walker, W.L., Tian, Y., Xu, H., Adamczy, P., Zhan, X., Liu, D.Z., Ander, B.P., Liao, I.H., Gregg, J.P., Turner, R.J., Jickling, G., Lit, L., Sharp, F.R. (2009) Identification and validation of suitable endogenous reference genes for gene expression studies in human peripheral blood. BMC Medical Genomics, 2:49 .

Turner, R.J., Vink, R. (2007) Inhibition of neurogenic inflammation as a novel treatment for ischemic stroke. Drug News and Perspectives, 20:221-6.

Donkin, J., Turner, R.J., Hassan, I., Vink, R. (2007) Substance P in traumatic brain injury. Progress in Brain Research, 161:97-109.

Turner, R.J., Blumbergs, P.C., Sims, N.R., Helps, S.C., Rodgers, K.M., Vink, R. (2006) Increased substance P immunoractivity and edema formation following reversible ischemic stroke. Acta Neurochir (Suppl), 96:263-266.

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