The Effect Of Metals On Neurofibrillary Tangle Formation
Funder
National Health and Medical Research Council
Funding Amount
$333,313.00
Summary
The majority of studies into Alzheimer's disease (AD) have focussed on two brain lesions- the plaque and neurofibrillary tangle (NFT), which are believed to have a causative role in AD. Our lab has made several seminal discoveries about the role that metals play in the development of plaques. We are now extending this work to evaluate the role of metals in NFT formation. These studies will provide insight into the formation and possible treatments for this primary brain lesion in AD.
Novel Treatment Approaches To Prevent Joint Fusion In Ankylosing Spondylitis
Funder
National Health and Medical Research Council
Funding Amount
$477,440.00
Summary
Ankylosing spondylitis (AS) is a form of arthritis targeting the spine and pelvis that causes uncontrolled bone formation resulting in complete joint fusion, severe disability and even death for which no therapies are currently available. Using a mouse model that closely replicates the human disease we will characterise the changes causing this joint fusion and identify possible new targets to develop novel treatments.
The Genetic Control Of Platelet Production And Function
Funder
National Health and Medical Research Council
Funding Amount
$558,920.00
Summary
Platelets are the tiny cells that circulate in the body and make blood clot. The human body has more than a trillion of them at any one time, and they are replaced every week by the blood producing cells that reside in the bone marrow. Keeping the normal number of platelets steady is incredibly important any significant drop can result in a life-threatening hemorrhage. The clinical name given to a low platelet count is thrombocytopenia, and it is a very common problem. It can be caused by geneti ....Platelets are the tiny cells that circulate in the body and make blood clot. The human body has more than a trillion of them at any one time, and they are replaced every week by the blood producing cells that reside in the bone marrow. Keeping the normal number of platelets steady is incredibly important any significant drop can result in a life-threatening hemorrhage. The clinical name given to a low platelet count is thrombocytopenia, and it is a very common problem. It can be caused by genetic mutations, viral infections, or by cancer treatments like chemotherapy. The only way to raise platelet numbers in a person with thrombocytopenia is a blood transfusion, which carries with it risks and potential side effects. While we understand quite a lot about how the body produces platelets, we don t know anywhere enough to be able to develop new treatments. Our work is focused on the identification of the genes that control the process, beginning with mouse models of thrombocytopenia, genome mapping, gene isolation, and finally, making the links between the newly identified genes and patients with thrombocytopenia. It will give us a much better understanding of how platelets are produced, how things go wrong in human disease, and how new therapies might be developed to treat them.Read moreRead less
Slowing Progression Of Alzheimer’s Disease By Modulating The Kynurenine Pathway
Funder
National Health and Medical Research Council
Funding Amount
$578,460.00
Summary
Chronic inflammation in the brain in known to be a factor in the progression of Alzheimer's disease. We are exploring if blocking a particular enzyme in a biochemical pathway involved in inflammation, can improve symptoms, or slow progression, of the disease in animal models of AD. If results are as expected, our proposal has the potential to generate a new a therapy for AD.
Nedd4-2: A New Player In Polycystic Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$671,995.00
Summary
Polycystic kidney disease (PKD) is a life threatening disorder affecting over 12 million people worldwide. This project is based on our discovery of a new gene that controls PKD. Using kidney specific gene knockout, biochemical and cellular approaches we will now address how this gene controls PKD. The results from this study will lead to better understanding of the underlying mechanisms that cause PKD, thus providing possible new targets for therapeutic interventions.
In Vivo Investigation Of Human PR3 Transgenic Mice: A Novel Animal Model To Understand The Role Of PR3 In Chronic Inflammation And Autoimmune Vasculitis
Funder
National Health and Medical Research Council
Funding Amount
$378,615.00
Summary
Granulomatosis with polyangiitis (GPA) is a form of vasculitis and is associated with antibodies directed against proteinase 3 (PR3). PR3 is expressed in neutrophils, monocytes and macrophages and has a number of well-characterized pro-inflammatory functions. The aim of this project is to understand the role of PR3 in inflammation and autoimmune vasculitis in vivo. This will be achieved using a transgenic mouse model expressing human PR3.
The majority of stroke results from focal brain infarction, followed by substantial secondary excitotoxic damage in the surrounding areas. Tau has been shown to contribute to excitotoxicity and neurodegeneration in mouse models of Alzheimer’s disease (AD). Preliminary data show that tau reduction also protects against excitotoxic damage after experimental stroke. We aim to dissect the molecular mechanisms of stroke using a tau-deficient mouse model.