Acute And Chronic Stroke - Novel Imaging Biomarkers Of The Ischemic Penumbra And Recovering Infarct
Funder
National Health and Medical Research Council
Funding Amount
$105,388.00
Summary
Stroke is a major cause of death and disability in our community. Most strokes result from a blocked blood vessel in the brain which leads to the almost immediate death of some brain tissue. However surrounding brain tissue is potentially salvageable if blood supply can be restored. This research uses magnetic resonance imaging (MRI) to better demonstrate salvageable brain tissue so that existing treatments to re-open blocked blood vessels can in future be safer and more widely applicable.
Raised Intracranial Pressure After Trauma: Characterisation And Development Of Pharmacological Interventions
Funder
National Health and Medical Research Council
Funding Amount
$589,788.00
Summary
Raised intracranial pressure (ICP) commonly occurs after traumatic brain injury (TBI) and is thought to be responsible for up to 50% of all mortality, as well as significantly contributing to the persistent neurological deficits in survivors. Few studies have examined the dynamics of raised ICP after TBI, or its effects on brain oxygenation. This study will fully characterize changes in ICP and brain oxygen after TBI and develop novel treatments to control such changes.
Characterisation Of Antioxidant Pathways Involving Gpx-1: Implications For Neural Ischemic Reperfusion Injury.
Funder
National Health and Medical Research Council
Funding Amount
$458,250.00
Summary
Neural damage following stroke can be grouped into two stages. The first occurs immediately following the ischemic insult and results in the rapid loss of neural cell viability; the second stage (which usually results in severe neural dysfunction) occurs over many hours following reperfusion. There is however, a window of opportunity shortly following the ischemia-reperfusion where damage to the brain can be minimized if appropriate therapeutic intervention was available. However, our ability to ....Neural damage following stroke can be grouped into two stages. The first occurs immediately following the ischemic insult and results in the rapid loss of neural cell viability; the second stage (which usually results in severe neural dysfunction) occurs over many hours following reperfusion. There is however, a window of opportunity shortly following the ischemia-reperfusion where damage to the brain can be minimized if appropriate therapeutic intervention was available. However, our ability to identify novel targets and devise strategies for the treatment of stroke relies on our understanding of (a) the molecular processes that are initiated following brain ischemia and (b) the delayed molecular events that follow reperfusion and hypoperfusion and result in extensive neuronal loss. A major component that accompanies stroke is the generation of oxidative stress. Reactive oxygen species (ROS) are thought to make a significant contribution to neuronal cell injury and death during both the early and late stages following ischemia. Therefore the molecular pathways that are involved in ROS generation are prime targets for the development of improved therapies. It has already been established by us that the antioxidant enzyme, glutathione peroxidase-1 (Gpx-1) is essential in protecting neurons from ischemic injury-death. A clearer understanding of how Gpx-1 confers this protection in vivo would make an important contribution towards the design of improved treatments. In this proposal, we plan to determine the role of Gpx-1 in an in vivo model of stroke to: (1) demonstrate in a broader sense the functional importance of this antioxidant enzyme in neuronal survival and (2) to demonstrate in a more specific manner, the impact of this enzyme on two signaling molecules, PI3kinase (PI3K) and NFkB (both of which are redox sensitive and play important roles in neuronal cell viability) and their relevance to ischemic cell injury and death.Read moreRead less