|Associate Professor Peter Crackemail@example.com||61 3 8344 8417||View page|
Stroke is the leading cause of long-term disability in adults and ranks as the third leading cause of death after heart disease and cancer. Approximately 80% of all strokes suffered are ischemic, resulting from artery occlusion and causing absent perfusion at the core of the infarct and hypoperfusion at the margin of the blood vessels territory (penumbra). The extent of neurological damage following stroke and the severity of the neurological sequelae depend on the viability of the hypoperfused penumbra and also on whether artery occlusion is transient, resulting in reflow (reperfusion). Hypoperfusion and reperfusion is accompanied by the production of reactive oxygen species (ROS) or free radicals at an enhanced rate. In turn, ROS trigger molecular pathways that lead to necrosis, apoptosis and neuroinflammation with subsequent neuronal loss and consequent disability. The devastation of stroke could be greatly ameliorated if therapies were available to salvage these potentially viable neurons. Therefore the molecular pathways that are involved in ROS generation and neuronal cell injury following ischemia are a prime target for the development of improved therapies.
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