Over 72,000 Australians suffer a stroke each year, with two-thirds left dead or disabled. There’s never been a more important time to fund research into brain aneurysm and stroke prevention and treatment.

1 in 4 adults globally will experience a stroke during our lifetime but 90% of these strokes can be prevented by addressing a few key risk factors, such as high blood pressure (hypertension), irregular heartbeat (atrial fibrillation), smoking, diet, and exercise.

Your donation can help researchers develop more effective stroke treatments, as well as how to reduce brain swelling and pressure that cause death and disability after stroke.

Donate to Stroke Research now.

2023 Research Funded:

Characterising Local Fibrinolysis in Chronic Subdural Haematoma Fluid (FiCS)

Funding: $25,980

Chronic Subdural Haematoma (cSDH) is an extremely common neurosurgical condition in which aged blood products collection on the brain surface beneath the skull, typically requiring surgical evacuation. cSDH prevalence is rising with our ageing population, and cSDH surgical evacuation is predicted to become one of the most encountered neurosurgical procedures by 2030. Up to 1/3 of patients undergoing cSDH evacuation will require repeat surgery due to recurrent bleeding, however, the pathways contributing to this are poorly understood. This study seeks to understand the haemostasic mechanisms that contribute to cSDH development, recurrence, and related surgical outcomes.

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Ms Lola Kaukas BHlthSci (Hons), GradCert

Research Officer, Department of Neurosurgery, Royal Adelaide Hospital

Investigating the ‘no reflow’ phenomenon in a clinically relevant model of stroke

Funding: $48,327

The most common cause of stroke (~85%) is blockage of a brain blood vessel by a clot (ischaemic stroke). The current goal of stroke treatment is to remove the clot from the vessel (recanalisation) and restore blood flow to the affected area (reperfusion) as fast as possible. However, despite successful recanalisation, many patients do not achieve adequate reperfusion, termed the ‘no reflow’ phenomenon, and this is associated with worse patient outcomes. This pilot study seeks to determine whether this phenomenon occurs in at risk, yet potentially salvageable brain tissue (penumbra).

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Dr Rebecca Hood, B. Biomedical Sci (Hons), PhD

Postdoctoral Research Fellow, School of Biomedicine, University of Adelaide

Developing an instrumented large mammalian model of delayed cerebral ischaemia
following subarachnoid haemorrhage

Funding: $49,751

Subarachnoid haemorrhage (SAH) is a type of stroke. It occurs when a blood vessel in the brain is weakened and ruptures leading to bleeding around, and into the brain. One in three people who have this type of stroke will die, and those that survive often have permanent brain injury. There are few treatments known to be effective for reducing mortality and improving long term outcomes following SAH. Our program will develop a world-first large animal model of SAH, providing the platform for pre clinical trials of novel therapies and a pathway for rapid translation to human studies.

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Dr Tim Webber MBBS FCICM, Intensive Care Medicine Fellow

Intensive Care Research Unit, Royal Adelaide Hospital

Equipment: Abbott iSTAT Analyser Wireless

Funding: $10,507

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The Abbott iSTAT Analyser Wireless is a state-of-the-art blood analyser used in many hospitals around Australia to provide real-time diagnostic information on patient's blood gases, particularly those in emergency care. Researchers at the University of Adelaide will be using this handheld, portable device to make sure that experimental conditions closely mimic the clinical scenario. This helps ensure their research is translationally relevant whilst they investigate a number of important neurological diseases including stroke and traumatic brain injury.

During surgical and emergency procedures its essential to ensure that arterial blood gases (the oxygen and carbon dioxide levels in the blood as well as the blood’s pH balance) remain within normal (physiological) levels. Variance outside of normal levels can worsen patient outcomes, therefore it is important to carefully monitor these parameters.

Dr Rebecca Hood, B. Biomedical Sci (Hons), PhD

Postdoctoral Research Fellow, School of Biomedicine, University of Adelaide


2022 Research Funded:

Disodium malonate for the treatment of post-stroke ischaemia reperfusion injury

Funding: $35,195

Ischaemic stroke is a leading cause of death and disability worldwide. Arising due to cerebrovascular occlusion, current treatment involves removing the blockage to reestablish blood flow to compromised brain tissue, however, this often paradoxically worsens injury. Recently the mitochondrial metabolite succinate has been identified as a key driver in ischaemia reperfusion injury (I/R) post stroke, mediating its effects through binding succinate dehydrogenase (SDH). Malonate, a competitive inhibitor of SDH has the potential prevent I/R injury post stroke and markedly improve patient outcomes. Following from a promising pilot study, this project seeks to comprehensively evaluate the efficacy of malonate for the treatment of post-stroke reperfusion injury in a clinically relevant model.

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Dr Annabel Sorby-Adams BHlthSc (Hons), PhD Visiting Research Fellow

University of Adelaide - Adelaide Medical School, Faculty of Health and Medical Sciences


2021 Research Funded:

A biobank (collection of biological samples) for diseases of the blood vessels of the brain and spinal cord to study how they develop and to find more effective treatments

Funding: $43,000

Research Area: Adult & Paediatric Stroke

Project: Disorders of blood vessels of the brain can cause devastating strokes which may be fatal or everely disabling. The mechanisms of their development are incompletely understood.

We propose to establish a biobank (collection of biological samples) to study the molecular basis of surgical neurovascular disease. Tissue samples will be collected from consenting patients during the course of their surgery for neurovascular conditions including: Cerebral aneurysms, Arteriovenous Malformations, Cavernomas, Arteriovenous fistula, Moya moya disease and spontaneous brain haemorrhage. By pairing the biobank with already established clinical neurovascular databases at the Royal Adelaide and Women’s & Children’s Hospitals, it is anticipated this biobank will facilitate studies into the pathological mechanisms of neurovascular disease.

Results of subsequent studies will inform development of novel diagnostic and therapeutic strategies for patients and their families. Pairing biobanks with large clinical database will undoubtedly reveal clinically significant measurable outcomes.

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Professor Leanne M Dibbens BSc(Hons), PhD Professor of Human Genetics

University of South Australia - Australian Centre for Precision Health, Clinical and Health Sciences

To determine if the presence of the dynamic spot sign on CT perfusion imaging is associated with brain haemorrhage expansion and in turn benefit from early surgery

Funding: $25,000

Project: Intracerebral haemorrhage (ICH) accounts for up to 15% of all strokes. Haematoma expansion occurs in a subset of patients of patients with ICH, and is associated with clinical deterioration, increased mortality and poorer functional outcomes.

This project will assess the ability of CTP dynamic spot sign to predict haematoma expansion and clinical outcome in a variety of subtypes of intracerebral haemorrhage. This will in turn determine which patients would benefit from early surgery to improve their outcome. We will also compare the sensitivity and specificity of the CTA spot sign and the CTP dynamic spot sign. CTP and CTA are currently standard of care in any major stroke centre such as the RAH for patients presenting with ICH, and no extra neuroimaging above standard care occurs during this project.

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Dr Christopher Ovenden, University of Adelaide

A novel therapy for ischaemia reperfusion injury post-stroke

Funding: $43,000

Project: Ischaemic stroke is a leading cause of death and disability worldwide. Arising due to cerebrovascular occlusion, current treatment involves removing the blockage to re-establish blood flow to compromised brain tissue, however, this often paradoxically worsens injury. Recently the mitochondrial metabolite succinate has been identified as a key driver in ischaemia reperfusion injury (I/R) post stroke, mediating its effects through binding succinate dehydrogenase (SDH).

Malonate, a competitive inhibitor of SDH has the potential prevent I/R injury post stroke and markedly improve patient outcomes. This project aims to evaluate malonate in a pre-clinical stroke model to enhance translation from pipette to patient.

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Dr Annabel Sorby-Adams BHlthSc (Hons), PhD Visiting Research Fellow

University of Adelaide - Adelaide Medical School, Faculty of Health and Medical Sciences

Stroke Research:

The stroke research team, led by Assoc Prof Renée Turner, is using novel, pre-clinical models to map the development of brain swelling and changes in brain pressure following stroke in order to develop targeted and more effective treatments to reduce the devastating morbidity and mortality associated with these conditions.

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Assoc Prof Renee Turner and Assoc Prof Lyndsey Collins-Praino

University of Adelaide

Pericytes and the blood-brain barrier – key drivers of neurodegeneration following stroke?

Funding: $76,629 - Perpetual

Project: The current project will investigate whether pericyte migration and activity contribute to secondary neurodegeneration following stroke. In order to investigate this question, the project will involve three specific aims:

1. To determine the early (primary stroke lesion) and late (secondary neurodegeneration) loss of brain tissue that occurs following stroke in two different experimental models of stroke.

2. To characterise the changes in pericyte migration and activity up to 3 months following stroke.

3. To assess whether alterations in pericytes are related to increases in levels of key neurodegenerative and neuroinflammatory markers in brain tissue post-stroke.

Assoc Prof Renee Turner

University of Adelaide

Can we use the brains’ own protective mechanisms to treat stroke?

Funding: Coopers Brewery Foundation Golf Day 2019 $142,400

sAPPa is a molecule that is found naturally in the brain and levels are increased in response to injury as a protective response. Can administered sAPPa salvage brain tissue and improve outcome following stroke? This project seeks to determine whether administering this protein after stroke can reduce the amount of brain tissue injured, facilitate recovery and improve patient outcomes. Our project will rigorously test the efficacy of sAPPa for the treatment of stroke in both small and large animal models of stroke. From these findings we will be able to inform on the suitability of sAPPa as stroke treatment and whether advancement to clinical trials is warranted.

Assoc Prof Renee Turner

University of Adelaide

The role of pericytes in delayed post-stroke neurodegeneration

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.

Annabel Sorby-Adams research is looking at that brain swelling and increased brain pressure which are the leading causes of death and disability in the first week following stroke. Annabel’s investigations will examine the effect of a treatment, the NK1 tachykinin receptor antagonist and whether it can prevent the development of brain swelling and life threatening elevations in brain pressure.

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