Viral Targeting Of STAT Proteins: Roles In Disease
Funder
National Health and Medical Research Council
Funding Amount
$536,985.00
Summary
The capacity of viruses to evade the host immune response is critical to the development of disease. We recently showed that interaction of specific viral proteins with host immune proteins called STATs is vital to lethal disease caused by lyssaviruses. In this project, we aim to define in detail the functions of these interactions in viral modification of host biology and evasion of the immune response, and to use this information to develop new vaccines against highly pathogenic human viruses.
Understanding Neuroinflammation In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$1,043,216.00
Summary
This project opens a new line of enquiry into the cellular signalling mechanisms involved in the progression of AD and establishes whether targeting the involvement of type-1 IFN signalling influences the evolution of AD. New and novel approaches are clearly required to treat AD. Importantly, we believe that neuroinflammation is common to all causes of dementia and targeting the neuroinflammatory pathways has much wider implications than targeting the primary causative pathway.
Controlling Neuroinflammation In Alzheimer's Disease
Funder
National Health and Medical Research Council
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide, with 269,000 Australians currently diagnosed with AD and is expected to soar to about 981,000 by 2050. AD accounts for greater than 60% of all cases of dementia. This grant investigates the role that neuroinflammation plays in the progression and exacerbation of AD and will identify new therapeutic strategies to combat this insidious disease.
Interleukin 38: Uncoupling Innate Inflammation From Interferons In Lupus
Funder
National Health and Medical Research Council
Funding Amount
$1,048,669.00
Summary
Systemic lupus erythematosus (SLE) is an incurable autoimmune disease that affects 5 million patients worldwide, mostly young women. Grave multi-organ inflammation and substantial loss of life expectancy render SLE a critical unmet medical need. We found that the immune system protein interleukin 38 disables several signalling pathways essential for SLE progress. We will explore regulation and function of this protein in cells from healthy people and SLE patients and in models of the disease.
Anti-viral Immunity In Asthma: A Detailed Assessment Of TLR7 Function And The Regulation Of Interferon ?/? Synthesis.
Funder
National Health and Medical Research Council
Funding Amount
$517,156.00
Summary
Many people with asthma are unusually vulnerable to viral infections. This study will carefully examine different components of immune function in people with asthma, including the receptors that respond to viral nucleic acids and the reasons why people with asthma do not produce normal quantities of anti-viral interferons. This research may lead to novel methods for prevention and treatment of virus infections in people with asthma.
Investigating Type I Interferon-mediated Immune-suppression During Plasmodium Infection
Funder
National Health and Medical Research Council
Funding Amount
$561,617.00
Summary
Some infections tend to afflict us only once in our lifetimes, for example chickenpox. This is because our bodies develop immunity to these infections relatively easily. The same is not true for malaria. It is thought that our immune systems are somehow suppressed during this disease. This project aims to understand how the immune system is suppressed during malaria infection, in order that we can block this process, and help our bodies fight this disease more effectively.
Antiphospholipid Syndrome Related Thrombosis: Understanding The Disease Pathogenic Mechanisms Is The Key To Better Diagnosis And Treatment
Funder
National Health and Medical Research Council
Funding Amount
$607,497.00
Summary
Patients with the Antiphospholipid Syndrome develop thrombosis at a young age. It requires long-term treatment with blood thinning medications, which have risks of severe bleeding. Methods are needed to decide which patients require long term treatment, avoiding unnecessary treatment in low risk patients. Such methods do not currently exist. In this study we explore how useful two novel assays developed by us are in identifying which of these patients are at high risk of thrombosis.
Testing The Prion Hypothesis In Parkinson’s Disease Using A Novel In Vivo Model Of Α-synuclein Transmission
Funder
National Health and Medical Research Council
Funding Amount
$622,555.00
Summary
Parkinson’s Disease (PD) is a debilitating neurological disease with no cure. Recently it has been discovered that the disease can spread through the brain. We have developed the worlds first animal model to study exactly how the disease propagates inside of neurons during this spread. We will use the model to answer key questions about this critical stage of disease spread, knowledge that is essential for the development of successful therapies to prevent disease progression.
The Role Of Redox-related Post-translational Changes Of Complement Factor H (CFH) In Age-related Macular Degeneration
Funder
National Health and Medical Research Council
Funding Amount
$652,019.00
Summary
Patients with AMD experience loss of central vision and this disorder is the leading cause of blindness in those aged over 50 years in Australia. There are currently no effective treatments for dry AMD. We have identified a protein that undergoes a modification in the blood and the eyes of humans with AMD that has given us new insights into how AMD develops. Specific therapies targeting this modified protein may offer a new treatment for this important cause of blindness.
Therapeutically Targeting The Major Genetic Risk Factor Of Alzheimer’s Disease
Funder
National Health and Medical Research Council
Funding Amount
$530,069.00
Summary
The second greatest risk factor for Alzheimer’s disease (after age) is genetic variation in a protein called APOE, however it is unknown why APOE increases the risk of disease. We have new clinical and laboratory evidence that APOE incresase risk of Alzheimer’s disease by manipulating iron pathways in the brain. We plan to examine these pathways and apply a new theraputic we have developed that targets these pathways in animal models of Alzheimer’s disease.