Molecular Mechanisms That Help Organise Effective Synaptic Transmission.
Funder
National Health and Medical Research Council
Funding Amount
$555,825.00
Summary
This study will test the idea that adhesion molecules alpha4- and beta2-laminin are needed for proper development and function of motor nerve - muscle connections. This study will provide insights into how such molecules control effective nerve-muscle communication, in both health and disease. We also believe that our results will provide the basic knowledge needed for identifying pharmacological targets that could improve such connections, and to promote reconnections between nerve and muscle.
The Role Of Neuronal Hyper-excitability In An Animal Model Of Motor Neuron Disease
Funder
National Health and Medical Research Council
Funding Amount
$558,170.00
Summary
Every day at least one person in Australia dies of the fatal and untreatable adult neurodegenerative disease of amyotrophic lateral sclerosis (motor neuron disease). This research examines the factors driving early increases in neural activity which may lead to the loss of upper and lower motor neurons in adulthood. The use of new methods to suppress production of specific proteins causing increased neural activity may lead to novel treatments for this disease.
How Does The P75 Neurotrophin Receptor Transmit Both Pro-survival And Pro-apoptotic Signals In Neurons?
Funder
National Health and Medical Research Council
Funding Amount
$265,500.00
Summary
Signaling by the two NGF receptors, TrkA and p75, determines the survival or death of sensory neurons and of certain brain neurons involved in memory and learning. The most baffling aspect of these receptors is that in most circumstances they cooperate with each other to maximise the survival of neurons when NGF is present, but in some situations they are opposed to each other. In the latter case, NGF treatment can lead to death, rather than rescue, of neurons. In the last three years we have de ....Signaling by the two NGF receptors, TrkA and p75, determines the survival or death of sensory neurons and of certain brain neurons involved in memory and learning. The most baffling aspect of these receptors is that in most circumstances they cooperate with each other to maximise the survival of neurons when NGF is present, but in some situations they are opposed to each other. In the latter case, NGF treatment can lead to death, rather than rescue, of neurons. In the last three years we have developed novel antisense oligonucleotides which can be used to switch off each receptor separately. These have been, and will continue to be, particularly valuable tools for our research. We have also uncovered a novel way in which the two receptors interact (via a signal transduction molecule known as SHC), which provides us with a competitive edge in this area. We have the expertise and equipment to identify and clone the missing factors that account for the paradoxical interactions between p75 and TrkA. A successful outcome from this project will have important benefits by improving our understanding of the factors controlling neuronal fate, and will help to develop treatments for neurodegenerative diseases.Read moreRead less