Stroke affects ~60,000 Australians every year and is a leading cause of disability. Approximately 80% of all strokes suffered are ischaemic, resulting from artery occlusion and causing a lack of perfusion at the core of the infarct and reduced perfusion at the margin of the blood vessels territory (penumbra). Cellular and molecular pathways triggered from the occlusion lead to necrosis, apoptosis and neuroinflammation with subsequent neuronal loss. Currently, there are no clinically effective neuroprotective agents that can be administered post-injury to prevent neuronal death. Our aim is to develop and evaluate therapies to target cellular and molecular pathways that are involved in neuronal cell injury following ischaemia.