Targeting Early Cellular Damage During Secondary Degeneration Using Nanosphere-based Drug Delivery
Funder
National Health and Medical Research Council
Funding Amount
$424,407.00
Summary
After brain injury, there are no treatments to stop the spread of damage to intact tissue, a process involving different cell types and biochemical events. Clinical trials have targeted one event and have failed because large therapeutic doses are toxic and because combined treatments are needed to target different events. We will harness nanotechnology to target delivery of small, sustained doses of one or more drugs to specific cell types and biochemical events to stop the spread of damage.
Molecular Mechanisms And Pharmacology Of The Dynamins
Funder
National Health and Medical Research Council
Funding Amount
$883,375.00
Summary
His research focuses on the molecular mechanisms of synaptic transmission in the nervous system to: a) understand the basic science of nerve communication and b) develop drugs to control diseases of nerve terminals like epilepsy. The main focus is on proteins called the dynamins, which are self-assembling molecular machines acting in many intracellular functions. There are three dynamin genes: dynI, II and III with diverse functions in the different parts of the body.
Metabolism And Neurotoxicity Of Hemin And Hemin-derived Iron
Funder
National Health and Medical Research Council
Funding Amount
$346,400.00
Summary
Stroke is a leading cause of death and disability in industrialised countries. Much of the brain damage that follows a hemorrhagic stroke is attributable to the presence of free iron which mediates oxidative stress in brain cells. This iron originates from hemin, which in turn is derived from the hemoglobin in extravasated blood cells. The fact that iron is freed from hemin in the post-stroke period makes it an attractive therapeutic target. However, remarkably little is known about the metaboli ....Stroke is a leading cause of death and disability in industrialised countries. Much of the brain damage that follows a hemorrhagic stroke is attributable to the presence of free iron which mediates oxidative stress in brain cells. This iron originates from hemin, which in turn is derived from the hemoglobin in extravasated blood cells. The fact that iron is freed from hemin in the post-stroke period makes it an attractive therapeutic target. However, remarkably little is known about the metabolism of hemin by the different types of brain cells. The present project investigates the metabolism and neurotoxicity of hemin in brain cells and will examine the capacity of potential therapeutic agents to protect brain cells from hemin toxicity. The data obtained from this project will advance our understanding of the uptake and metabolism of hemin by the four main types of brain cell, and the factors that are likely to be involved in the neurotoxicity of hemin-derived iron following hemorrhagic stroke. The study will also provide data concerning the relative effectiveness of potential therapeutic agents, and information concerning the cell types, time points and aspects of hemin metabolism that are most effectively targeted by these agents. Such advances will guide the development of therapeutic approaches that are directed at minimising the brain damage which results from hemin-derived iron in humans.Read moreRead less