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To Investigate How The Aggregation Of Proteins During Neuronal Injury Promotes Neurotoxic Plasmin Formation
Funder
National Health and Medical Research Council
Funding Amount
$586,428.00
Summary
tPA is an enzyme given to patients to remove stroke-causing blood clots but can have harmful effects in the brain. tPA needs a cofactor to function optimally. In the blood, this cofactor is fibrin. However the cofactor that allows tPA to function in the brain is unknown. This project explores a novel cofactor for tPA in the injured brain. We will attempt to block this harmful cofactor in the brain while still allowing tPA to remove clots thereby improving stroke outcome.
NPY Coordination Of Energy Balance And Physical Activity
Funder
National Health and Medical Research Council
Funding Amount
$844,596.00
Summary
Anorexia nervosa (AN) is an eating disorder characterized by behavioral alterations, restrictive eating leading to extremely low body weight. AN is also associated with a paradoxical hyperactivity representing a failure of the brain to adjust activity to energy status. Here we aim to investigate the role of the Neuropeptide Y (NPY), a known regulator of homeostatic control and activity in the development of hyperactivity in AN, thus help to identify NPY-targeted therapeutics for AN treatment.
Sweet taste is generally associated with calorie rich diet. In the brain this information is used to adjust the amount of food that is eaten and how hungry one feels. Disrupting this balance by supplementing food with artificial sweeteners, which have no caloric content, represents a challenge for the brain. However, specific neuronal pathways are in place to correct this imbalance of calorie to taste and we are interested to identify the major component of these pathways.
Delayed Neuronal Death After Peripheral Nerve And Spinal Cord Injury
Funder
National Health and Medical Research Council
Funding Amount
$457,267.00
Summary
After injury to the nervous system, even under optimal conditions for regeneration of broken nerve processes (axons), there is little chance of normal function being restored because few regrowing axons will find appropriate cells to connect with. The time taken for many regrowing axons to reach their targets can be so long that both the axons and their targets lose the ability to recognize each other. Equally importantly, some damaged nerve cells die over the months that follow an injury. This ....After injury to the nervous system, even under optimal conditions for regeneration of broken nerve processes (axons), there is little chance of normal function being restored because few regrowing axons will find appropriate cells to connect with. The time taken for many regrowing axons to reach their targets can be so long that both the axons and their targets lose the ability to recognize each other. Equally importantly, some damaged nerve cells die over the months that follow an injury. This slow loss of nerve cells can lead to progressive and ongoing deterioration. Given recent advances in our understanding of how to improve axon regeneration, the degree of functional recovery could be disappointing unless we know more about how to prevent these neurones from dying. This project will use rats as experimental animals to try to understand which types of nerve cells are likely to die or survive after injury to peripheral nerve trunks or to the spinal cord. We will investigate two regions of the nervous system that are commonly involved in injuries in people. After injuries to limb nerves, people lose sensation and movement and can unpredictably develop chronic conditions such as neuropathic pain (unrelated to the damage and often occurring spontaneously) as well as poor blood flow and wound healing in the hands-feet. After most injuries to the spinal cord, the lower part of the cord beyond the injury (in particular the lumbosacral cord controlling hindlimb movement and sensation and the function of bladder, bowel and sexual organs) is often disconnected from the brain leading to paralysis and disrupted control of pelvic organ function. We will identify and study specific populations of nerve cells with sensory (mainly pain-sensing) functions and four identified groups of nerve cells in the lumbosacral cord that project to the brain. Once we know which nerve cells do not survive, we will search for the likely causes of their death and ways to prevent it.Read moreRead less
Functional Copper Deficiency Models Of Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$454,691.00
Summary
Alzheimer's disease is a serious neurodegenerative disease which increases in incidence with age. It affects the quality of life and care required for approximately 160,000 Australians and costs the national economy 6.6 billion dollars per annum. Current therapy is of limited efficacy. Our studies are directed towards testing the hypothesis that a functional deficiency of the essential trace element, copper, occurs in the brain with ageing, and this leads to oxidative stress and death of neurons ....Alzheimer's disease is a serious neurodegenerative disease which increases in incidence with age. It affects the quality of life and care required for approximately 160,000 Australians and costs the national economy 6.6 billion dollars per annum. Current therapy is of limited efficacy. Our studies are directed towards testing the hypothesis that a functional deficiency of the essential trace element, copper, occurs in the brain with ageing, and this leads to oxidative stress and death of neurons associated with Alzheimer's disease. We will use animal and cell culture models to test this hypothesis which is based on promising preliminary data from such models. We believe that beta amyloid, which accumulates in Alzheimer's brains and is believed to be a major part of the pathological mechanism, has a normal role in maintaining copper balance and that this balance is disturbed by ageing or particular mutations. This research should lead to better treatments using drugs which mobilise copper entry into cells.Read moreRead less