The Role Of Store-operated Calcium Entry In Neuronal Development
Funder
National Health and Medical Research Council
Funding Amount
$353,140.00
Summary
Defects in brain development can manifest in a range of disorders including autism and mental retardation. The highly complex, precise network that is our nervous system forms during development. Our work will determine the role of key proteins in guiding developing neurons. Understanding the function of such proteins will improve our ability to predict the outcome caused by mutations in these proteins, in the developing foetus.
The research outlined in this application seeks to examine the role of calcium in the pathogenesis of AD. It will examine the hypothesis that the build-up of a protein known as the Abeta causes an increase in levels of calcium in nerve cells of the brain. This increase in calcium may trigger nerve cell damage and dementia. The ultimate aim of the research is to identify new targets for drug development in Alzheimer's disease.
Deciphering The Mechanisms Underlying LRP-mediated Axon Guidance
Funder
National Health and Medical Research Council
Funding Amount
$370,659.00
Summary
Nerve damage can develop post injury or disease and are often very debilitating, slow to heal and cause increased pain. Our work aims to examine a new class of molecules that we show can activate selected fat-receptors on nerve cells to guide the growth of regenerating nerves. We will determine how these receptors function with the aim of developing a novel class of therapeutics directed at healing nerve damage.
Learning And Network Plasticity In A Primitive Sensory Cortex
Funder
National Health and Medical Research Council
Funding Amount
$461,557.00
Summary
Our brain is a uniquely powerful supercomputer, in part because it is ‘plastic’ -- that is, it can change itself when we adapt or learn something new. An understanding of the causes of brain plasticity is an essential part of any quest to understand the brain in sickness and in health. This research uses a laser microscope to ‘read the minds’ of mice as they learn about odours. By observing plasticity in action, we will gain deeper insights into normal brain function.
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.
Role Of The Microglial Adaptor Molecule TYROBP In Alzheimer’s Disease Pathology
Funder
National Health and Medical Research Council
Funding Amount
$469,433.00
Summary
Immune activation characterizes Alzheimer’s disease (AD) brains; however, how it impacts AD progression is not understood. Our previous studies in AD brains identified the immune molecule TYROBP, pointing at both beneficial and detrimental effects triggered by this molecule. Here, we aim to understand in detail how TYROBP is involved in AD and how we can enhance its beneficial effects and decrease its unintended actions.
Wnt-Ryk Signaling In The Establishment Of Major Axon Tracts In The Embryonic Mouse Brain
Funder
National Health and Medical Research Council
Funding Amount
$513,946.00
Summary
The corpus callosum is the major interhemispheric commissure in the human brain, comprising approximately 3 million myelinated fibers which connect homologous regions in the neocortex. To date more than 50 different human congenital syndromes have been described in which the corpus callosum does not form leading to epilepsy and mental retardation. We have identified a new guidance molecule (Ryk) which is crucial for corpus callosum formation. This project aims to dissect that molecular mechanism ....The corpus callosum is the major interhemispheric commissure in the human brain, comprising approximately 3 million myelinated fibers which connect homologous regions in the neocortex. To date more than 50 different human congenital syndromes have been described in which the corpus callosum does not form leading to epilepsy and mental retardation. We have identified a new guidance molecule (Ryk) which is crucial for corpus callosum formation. This project aims to dissect that molecular mechanisms controlling Ryk signaling during corpus callosum development. Our analysis of Ryk function will advance our understanding of the molecular mechanisms underlying the formation of this important commissure.Read moreRead less
Aberrant Ependymal Development And The Formation Of Hydrocephalus
Funder
National Health and Medical Research Council
Funding Amount
$660,005.00
Summary
Foetal hydrocephalus is a prevalent neurodevelopmental condition associated with severe intellectual impairment. Breakdown of the ependymal cell layer, which acts as a barrier between brain tissue and the ventricular space, is a major cause of hydrocephalus. Despite the importance of these cells, we have little understanding of the molecular mechanisms that regulate their production. This project will identify critical signalling pathways governing the establishment of the ependymal layer.
Axonal Fusion To Promote Nerve Repair: Molecules And Mechanisms.
Funder
National Health and Medical Research Council
Funding Amount
$456,189.00
Summary
Nerve injuries are in most cases untreatable, leaving patients with high level of disabilities for the rest of their life. Understanding the molecular mechanism regulating nerve regeneration is critical to develop new drugs and design innovative therapies. We discovered molecules that mediates axonal repair by favouring the stitching together of the two separated fragments of an axon. We aim to study how they functions to possibly exploit a similar mechanism of repair for human injuries.
Is Kainate Receptor Dysfunction At The Core Of Multiple Sclerosis Neuropathology?
Funder
National Health and Medical Research Council
Funding Amount
$318,768.00
Summary
Multiple Sclerosis (MS) is a devastating disease. The current treatments for MS are not able to prevent the death of cells in the brain and are not able to prevent disability in MS patients. I have identified a family of genes that I predict are responsible for cell death in MS. I will determine what these genes do in the brain. My aim is to identify a target for new treatments to prevent cell death in MS.