I use multidisciplinary and neuroimaging approaches to understand how the biochemistry of the brain affects how the brain functions in health and disease. This basic science underpins treatment approaches and furthers our understanding of a wide range of brain disorders.
Identifying Neuroanatomical Sub-phenotypes Of Schizophrenia
Funder
National Health and Medical Research Council
Funding Amount
$60,129.00
Summary
The clinical presentation of schizophrenia is varied across individuals, and has arguably hindered efforts to determine its cause/s. This project seeks to address this issue by investigating biological commonality in patients, to identify subgroups of schizophrenia patients with similar brain abnormalities, with the overall aim to examine cognitive and clinical characteristics and candidate genetic markers in association with biologically derived subtypes of schizophrenia.
Social Functioning In Early Primary School Following Traumatic Brain Injury Prior To Age Three: The Contribution Of Cognitive, Environmental And Neurological Factors
Funder
National Health and Medical Research Council
Funding Amount
$394,501.00
Summary
Children of preschool age and older demonstrate social problems after a traumatic brain injury (TBI). What effect a TBI has on the social function of young children (before 3 years) is currently unknown but is thought that these children have more problems than older children do. This study will look at how a TBI impacts on the social function of young children and the role of cognition and brain development in social function will also be explored.
Development And Epilepsy - Strategies For Innovative Research To Improve Diagnosis, Prevention And Treatment In Children With Difficult To Treat Epilepsy
Funder
National Health and Medical Research Council
Funding Amount
$456,083.00
Summary
By deciphering pathophysiological mechanisms in epileptogenic developmental disorders and developing mechanism-related, and advanced therapeutic strategies, we expect to discover novel genes and related molecular pathways that are involved in epilepsy and similar disorders. DESIRE will also help preventing the development of the disease after potentially epileptogenic brain insults.
Development Of A Scorpion Toxin For Tumour Imaging
Funder
National Health and Medical Research Council
Funding Amount
$529,577.00
Summary
The aim of this project is to develop a tool for visualising tumours during surgery. Surgical removal of tumours remains the foundation of cancer treatment, but the ability to distinguish the margin between cancerous and healthy cells is imprecise. We will explore the potential of a scorpion toxin that selectively targets cancer cells, as a tumour imaging agent. This project has the potential to dramatically enhance patient survival as a result of improving treatments for cancer.
Genetic And Environmental Determinants Of Brain Networks In Ageing
Funder
National Health and Medical Research Council
Summary
Is brain ageing genetically or environmentally determined, or an interaction of both? We will explore the influence of genes and the environment on brain connectivity during ageing by studying how the brain network relates to cognitive functions.
The Effect Of Anti-fibrinolytic Drugs On Blood-brain Barrier Integrity And The Immune Response In Traumatic Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$870,476.00
Summary
This project aims to determine how a well known anti-fibrinolytic drug can improve the immune response and reduced blood brain barrier disruption following traumatic brain injury. We will also be testing additional drugs we have developed as well as a novel drug delivery system that better targets drugs to the damaged brain.
APLP2: A Neuroprotective Receptor For Acute Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$648,739.00
Summary
Traumatic brain injury (TBI) is the major cause of deaths in Australians under 45 years of age. We have shown that the amyloid precursor protein (APP) is protective in models of TBI. To understand how APP is neuroprotective we have isolated APP binding proteins and identified the amyloid precursor-like protein 2 (APLP2) molecule as a strong candidate for the APP-neuroprotective receptor. This grant will investigate the interaction between APP and APLP2 as a novel neuroprotective pathway in TBI.
Role Of Post-traumatic Hypoxia In The Exacerbation Of Cerebral Inflammatory Response Elicited By Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$397,535.00
Summary
Traumatic brain injury is the major cause of death in the young population below the age of 40 years. Approximately 25% of patients that survive head injury remain with permanent neurological disabilities with considerable family, professional and economic costs. Extensive research has shown that not all brain damage occurs at the time of injury, but rather evolves over the hours and days following trauma. Secondary injury may result from various factors including hypoxia (insufficient oxygen) a ....Traumatic brain injury is the major cause of death in the young population below the age of 40 years. Approximately 25% of patients that survive head injury remain with permanent neurological disabilities with considerable family, professional and economic costs. Extensive research has shown that not all brain damage occurs at the time of injury, but rather evolves over the hours and days following trauma. Secondary injury may result from various factors including hypoxia (insufficient oxygen) as a consequence of respiratory distress that occurs in about 50% of patients with severe head trauma. Hypoxia is known to significantly worsen the neurological impairment and potentially lead to death. Brain injury and hypoxia have the ability to separately trigger cerebral inflammation. A dual role has been attributed to inflammation: to promote tissue repair but also add further damage through the release of neurotoxic substances. We hypothesise that hypoxia occurring after traumatic brain injury enhances the inflammatory response in the brain and aggravate tissue damage as well as neurological dysfunction. This hypothesis will be tested on a rat model of brain injury whereby the animals will be exposed to moderate-severe hypoxia immediately after trauma. The production of multiple inflammatory mediators will be quantified in the brain tissue and also in cerebrospinal fluid. The concentration of these mediators will be compared with the levels of cellular injury proteins known to increase following injury to determine whether a correlation exists. In a clinical study on patients, we will measure the same inflammatory mediators and proteins in the cerebrospinal fluid and blood of individuals with severe head injury. The suitability of these factors for potential use as diagnostic-prognostic markers of either hypoxia or injury will be determined.Read moreRead less