A/Prof Brad Sutherland
Associate Professor in Neuroscience
Head, Perivascular Research Group
Tasmanian School of Medicine
University of Tasmania
Brad completed his PhD at the University of Otago (Dunedin, New Zealand) where he investigated the activation of inflammatory pathways in the brain after stroke. After a small stint as a Teaching Fellow in Pharmacology & Toxicology (University of Otago), he took up a Post-doctoral Research Fellowship with the Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford (Oxford, UK). During his time in Oxford, he formed an interest in the regulation of blood flow in the brain in health and disease. This led to studies investigating the interaction between brain tissue and the blood vessels, the signalling mechanisms that controlled energy delivery to the brain, and how these were disrupted in conditions such as stroke. In mid-2016, Brad arrived at the University of Tasmania to build the Perivascular Research Group and continue investigating the control of cerebral blood flow and blood-brain barrier function with a focus on pericytes. He has a number projects investigating the dysfunction of the neurovascular unit in brain diseases such as stroke, Alzheimer’s disease, vascular dementia, multiple sclerosis and chronic fatigue syndrome. He has received >$10 million in research grant funding including multiple NHMRC and MRFF grants, and has made significant contributions to our understanding of the vascular contributions to neurological diseases. His lab uses a wide range of in vitro methods, in vivo models and human neuropathology to assess mechanisms of neurovascular regulation in health and disease.
Project Highlights
We are using in vitro and in vivo techniques to understand the role pericytes play in stroke pathophysiology and microvascular dysfunction. We are therapeutically targeting pericytes to prevent no-reflow in acute stroke and promoting vascular regeneration in the long-term to improve outcomes following stroke.
We recently identified that microglia make direct contact with pericytes and the cerebral vasculature which could have significant implications for vascular function. We are investigating the key functional roles these cellular interactions have, and how this may be altered in Alzheimer’s disease leading to impaired microvascular function.
We have recently identified significant deficits in the structure of the neurovascular unit in key areas vulnerable in multiple sclerosis. Due to the extensive inflammatory phenotype and consequences to neuronal structure and brain health, we are investigating the cellular mechanisms responsible for microvascular dysfunction in the context of multiple sclerosis.
Research Keywords
- Pericytes
- Cerebral blood flow
- Blood-brain barrier
- Neurovascular unit
- Microglia
- Stroke
- Alzheimer's disease
- Dementia
- Multiple sclerosis
- Animal models
- Cell culture
- Stem cells