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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.
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
The Role Of Urotensin II In Diabetes-Associated Atherosclerosis
Funder
National Health and Medical Research Council
Funding Amount
$405,594.00
Summary
People with diabetes most commonly die from stroke or heart attack and we need to determine what makes them more prone to these problems. The recently discovered UII system is increased in people with diabetes and has been found in diseased parts of blood vessels. Thus, the aim of this project is to characterise the UII system in the setting of diabetes using 2 unique genetically altered mice and a blocker a to study the effects of high cholesterol, diabetes and a deletion of UII.
Understanding The Genetic Determinants Of Central Corneal Thickness And Its Functional Role In Glaucoma Pathophysiology
Funder
National Health and Medical Research Council
Funding Amount
$297,263.00
Summary
Glaucoma is a common cause of blindness and visual diability in Australia. It is caused by a combination of environmental and genetic factors. People with a thin cornea (the clear covering at the front of the eye) are at increased risk of glaucoma. We are investigating the biological link between the cornea and glaucoma as well as identifying genes that determine corneal thickness. Some of these genes may also cause glaucoma. Understanding this will lead to better diagnosis and treatment.
The Role Of GRHL-3, A Mammalian Homologue Of Drosophila Grainyhead, In Neural Tube Development
Funder
National Health and Medical Research Council
Funding Amount
$496,500.00
Summary
Spina bifida and anencephaly are two common human congenital malformations that form part of a wide spectrum of mutations known collectively as neural tube defects (NTDs). Patients with the most severe form of spina bifida have a failure of the vertebral column and skin to close over the spinal cord and therefore suffer from limb paralysis and marked bladder and bowel dysfunction. Infants with anencephaly have an open cranial vault and failure of normal brain development and die within the first ....Spina bifida and anencephaly are two common human congenital malformations that form part of a wide spectrum of mutations known collectively as neural tube defects (NTDs). Patients with the most severe form of spina bifida have a failure of the vertebral column and skin to close over the spinal cord and therefore suffer from limb paralysis and marked bladder and bowel dysfunction. Infants with anencephaly have an open cranial vault and failure of normal brain development and die within the first few hours of life. These abnormalities occur frequently (1-1000 live births) and are a direct result of failure of the neural tube to close during embryogenesis. NTDs are influenced by both environmental and genetic factors. The best characterised environmental factor is the dietary supplement folate, which when administered before conception results in a reduction in the incidence of spina bifida. The genetic complexity is evidenced by the array of mouse genetic mutations that give rise to NTDs. One of these mouse mutations, known as Curly tail (ct), has served as the major animal model of human NTDs. This is because the ct mice are resistant to folate administration (like most of the cases of spina bifida currently seen in patients) and because the mice seem to have normal development in virtually all other organ systems. Ironically, the genetic mutation that causes the curly tail phenotype has remained undiscovered for over 50 years. We have now identified the gene mutated in the curly tail mice. This gene is highly conserved in humans suggesting that it will play a similar role in neural tube development in man. The gene, known as GRHL-3, is a descendant of a fly gene critical for development of the nervous system in that organism. The studies we propose here will examine the developmental pathways involved in normal neural tube closure in mice and humans and will impact on our understanding of these devastating congenital malformations.Read moreRead less
The Role Of The TGF-b Superfamily Cytokine MIC-1 In The Pathogenesis Of Atherosclerosis
Funder
National Health and Medical Research Council
Funding Amount
$348,950.00
Summary
MIC-1 is a protein first cloned and characterised by our research group. It belongs to the TGF beta protein superfamily which is very important in development, cancer, wound - fracture healing and inflammation. The aim of this project was to start to gain an understanding of the role of this protein, both in normal biological processes (especially pregnancy) and in disease. MIC-1 is present in the blood of all individuals and high levels are associated with an increased risk of heart attacks and ....MIC-1 is a protein first cloned and characterised by our research group. It belongs to the TGF beta protein superfamily which is very important in development, cancer, wound - fracture healing and inflammation. The aim of this project was to start to gain an understanding of the role of this protein, both in normal biological processes (especially pregnancy) and in disease. MIC-1 is present in the blood of all individuals and high levels are associated with an increased risk of heart attacks and strokes. In this study we wish to use animal models, in which the gene for MIC-1 has either been deleted or enhanced, to determine whether MIIC-1 plays a direct role in these diseases.Read moreRead less
Role Of The Ets Family Transcription Factor Erg In Stem Cell Function And Hematopoiesis
Funder
National Health and Medical Research Council
Funding Amount
$413,775.00
Summary
The cells responsible for producing blood are called hematopoietic stem cells (HSCs). Our research is focused on the genes that control HSC growth and development. We have discovered that a gene known to cause cancer, Erg, plays a critical role in regulating this process. This Project will tease apart the mechanism by which it does so, provide insights into how Erg can trigger cancer, and help us understand the molecular network of regulators that control blood cell production.
The Physiological Relevance Of Calcitonin In Osteoclast Function
Funder
National Health and Medical Research Council
Funding Amount
$437,640.00
Summary
Throughout adult life, bone tissue is continuously remodelled. The two main processes involved in bone remodelling, are bone formation and bone breakdown. Bone formation is controlled by cells known as osteoblasts and bone breakdown is controlled by cells known as osteoclasts. Under normal circumstances these two processes are tightly coupled. Excessive breakdown of bone, causes these two processes to become unbalanced and results in bone loss. This is the basis of many bone diseases such as ost ....Throughout adult life, bone tissue is continuously remodelled. The two main processes involved in bone remodelling, are bone formation and bone breakdown. Bone formation is controlled by cells known as osteoblasts and bone breakdown is controlled by cells known as osteoclasts. Under normal circumstances these two processes are tightly coupled. Excessive breakdown of bone, causes these two processes to become unbalanced and results in bone loss. This is the basis of many bone diseases such as osteoporosis, a condition in which the bones become fragile and therefore more susceptible to fracture. 1 in 2 women and 1 in 5 men aged 70 years and older suffer from osteoporosis in Australia. Despite this, the mechanisms which control osteoclast breakdown of bone are not well understood. Our laboratory is interested in how hormones affect osteoclast action. We plan to examine the role of the hormone calcitonin, thought to be important inhibitor of osteoclastic bone breakdown. This will be achieved by studying transgenic mice in which the receptor for calcitonin is specifically removed from osteoclasts. This will allow us to precisely determine the role of calcitonin in osteoclast function. Current treatment for osteoporosis involves the administration of drugs which inhibit bone breakdown. This project will increase our understanding of how calcitonin acts to regulate the function of osteoclasts. We believe that this research is of great importance as osteoporosis is becoming more prevalent as the population ages.Read moreRead less