Complement Activation As A Therapeutic Target And Clinical Biomarker For Parkinson's Disease
Funder
National Health and Medical Research Council
Funding Amount
$497,941.00
Summary
Parkinson’s disease is the second most common neurological disease in Australia, yet there is no treatment to slow disease progression. Our study is investigating inflammation within the brain as a major contributing factor in Parkinson’s disease. We will examine this inflammatory pathway in human patients suffering from Parkinson’s, and will test a novel anti-inflammatory drug in animal models of Parkinson’s disease, in order to identify a novel treatment to reduce disease pathology.
The Retina As A Chemogenetic Target For The Treatment Of Depression
Funder
National Health and Medical Research Council
Funding Amount
$408,768.00
Summary
Treatments for depression are often poor because they lack selectivity. By inserting receptors that respond to an inert drug, Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) can turn on-or-off very specific classes of cells, providing an exciting treatment direction for depression and other neuropsychiatric diseases. The long term goal of this project is to create a highly effective DREADD-based treatment for depression, which is activated by either eye drops or a pill.
Metal-mediated Mechanisms And Therapeutic Approaches For Treating Brain Injury Across Age
Funder
National Health and Medical Research Council
Funding Amount
$1,229,769.00
Summary
This grant will examine the role of zinc and iron in the neuronal changes that occur following brain injury, with a specific focus on the role of these metals in functional outcomes. We will also examine how the role of these metals changes across the normal lifespan, and also whether these metal changes are consistent across different types of brain injury. Finally, we will examine the therapeutic potential of zinc- and iron-targeted compounds.
Microtubule Stabilisation: Promoting Adaptive Plasticity, Brain Healing And Functional Recovery After Traumatic Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$507,258.00
Summary
Traumatic brain injury (TBI) continues to be the leading cause of death and disability for individuals under 45 years of age. There are currently no effective pharmacotherapeutics available that are able to prevent or minimise brain damage following TBI. My team will use sophisticated in vivo techniques to fully characterise the brain's response to injury and to test whether microtubule stabilisation via new generation taxol-like drugs improves post-trauma outcomes.
Therapeutic Targeting Of Neuroinflammation To Slow The Progression Of Neurodegenerative Disease
Funder
National Health and Medical Research Council
Funding Amount
$463,652.00
Summary
My research has identified key components of our immune system, that can worsen disease in conditions such as Parkinson’s disease and motor neuron disease. I hope that exploring these components in animal models, and patients suffering from these diseases, my group can identify new therapeutic drug candidates that can be progressed in clinical trials. Ultimately, this may lead to new treatments to reduce disease burden in patients suffering from these neurodegenerative conditions.
The Role Of BMP Signalling During Chronic Demyelination And Myelin Repair
Funder
National Health and Medical Research Council
Funding Amount
$67,381.00
Summary
Multiple sclerosis (MS) is the most common neurodegenerative disease affecting young adults. It is a disease that kills myelin cells, which are important support cells for neurons and critical for neuronal function. This research investigates the role of a specific signaling pathway with respect to myelin cell production and repair with the ultimate aim of identifying regenerative therapeutics for MS.
Characterisation And Modelling Of Schizophrenia-associated Dysregulation Of MiR-137 Expression
Funder
National Health and Medical Research Council
Funding Amount
$581,661.00
Summary
We have identified mutation-associated changes in the expression of a non-coding microRNA gene in the cerebral cortex in schizophrenia. This gene, known as MIR137, functions by repressing hundreds of target genes and therefore has major implications for schizophrenia. The project will identify the genetic mechanism affecting the expression of MIR137, and determine the biological and behavioural implications of this change in the context of schizophrenia.
Compromised Fetal Brain Development: Neurogenesis And The Potential For Therapeutic Intervention.
Funder
National Health and Medical Research Council
Funding Amount
$497,280.00
Summary
Lack of oxygen to the fetal brain during pregnancy is thought to be the main causes of brain injury in newborns. Some of these infants will suffer developmental and behavioural problems including cerebral palsy, schizophrenia and epilepsy. Currently, there is no effective treatment to redress these changes in brain development and this is one of the major challenges in perinatal medicine today. We have previously shown in a guinea pig model of chronic placental insufficiency (reduced oxygen and ....Lack of oxygen to the fetal brain during pregnancy is thought to be the main causes of brain injury in newborns. Some of these infants will suffer developmental and behavioural problems including cerebral palsy, schizophrenia and epilepsy. Currently, there is no effective treatment to redress these changes in brain development and this is one of the major challenges in perinatal medicine today. We have previously shown in a guinea pig model of chronic placental insufficiency (reduced oxygen and nutrient levels during pregnancy) that there is a reduction in neurons and in the connections between them. This may result from a reduction in number of newly generated neurons (neurogenesis), or an increase in neuronal death (apoptosis), or both. To develop therapeutic strategies to improve brain growth and ultimately functional recovery, we must understand the mechanisms which lead to these brain changes. In this project, we will use our guinea pig model to: 1) determine whether a suboptimal fetal environment decreases neuronal numbers by influencing neurogenesis, apoptosis or both, 2) study changes in the compromised brain environment which are likely to influence apoptosis and neurogenesis, 3) determine whether a suboptimal fetal environment has long-term effects on adult neurogenesis and 4) determine whether treatment with erythropoietin (Epo), a naturally occurring hormone, can resolve deficits in brain development and function. Epo is an exciting candidate as it is, or is in the process of being used to treat stroke and newborn asphyxiation. Epo has also been shown to prevent neuronal death and promote neurogenesis following brain injury. Understanding the mechanisms and finding effective treatments for brain damage is a vital area of endeavour if we are to help infants develop their maximum potential and reduce the enormous social, economic and educational burden which must be borne by the individual and society in general when things go wrong during pregnancy.Read moreRead less