Mitochondrial Damage Following Fetal Hypoxia Or Birth Asphyxia: Using Creatine To Preserve Mitochondrial Function
Funder
National Health and Medical Research Council
Funding Amount
$838,726.00
Summary
There is a need for a therapy that can be given before a mother gives birth to protect the baby should ‘oxygen starvation’ threaten the baby’s brain and other organs such as the heart, kidney, lungs, and the ability to breathe properly. We are suggesting that an increased intake of creatine is a very effective treatment against this threat, and its proven safety and ease of use recommends it for wide application, particularly in countries where the access to medical resources is poor.
Understanding Mitochondrial DNA Segregation And Transmission.
Funder
National Health and Medical Research Council
Funding Amount
$512,449.00
Summary
We inherit our mitochondrial DNA from our mothers. Mutations to mitochondrial DNA can give rise to severely debilitating diseases that can be passed from one generation to the next. The aims of this application are to understand how mutant mitochondrial DNA is selected for; when it affects energy production during development; and to ensure that certain reproductive strategies do not result in the adverse transmission of mitochondrial DNA that will affect subsequent generations.
Understanding The Pathogenesis Of Mitochondrial Disease Using IPS Cells
Funder
National Health and Medical Research Council
Funding Amount
$640,372.00
Summary
Induced pluripotent stem (iPS) cells are stem cells derived from adult skin cells that can be converted into cell types such as neurons. iPS cells offer great promise in understanding and treating inherited disorders. However, there are concerns that the “epigenetic memory” of iPS cells has not been completely erased, which may limit the utility of iPS cells. We will evaluate and validate the use of iPS technology in mouse and human models of inherited disorders affecting energy generation.
Metabolic And Molecular Basis Of Embryo Signalling
Funder
National Health and Medical Research Council
Funding Amount
$409,836.00
Summary
Cells in the body are powered by mitochondria that essentially generate the energy required for development. This grant will determine how the environment affects the mitochondria in the developing embryo and determine the impacts to the embryo and pregnancy if a mitochondria is partially shut down.
From Pathogenesis To Therapeutics: Targeting Two Signalling Pathways As A Therapeutic Strategy To Treat Preeclampsia
Funder
National Health and Medical Research Council
Funding Amount
$499,048.00
Summary
Preeclampsia is a serious complication of pregnancy that claims the lives of thousands of mothers and babies each year. There is no efficacious medical treatment besides delivery of the baby and placenta. Our lack of therapeutics is largely a result of our poor understanding of the disease. In this application we plan to thoroughly characterise two pathways we believe responsible for preeclampsia, effectively identifying many points at which new therapies could be targeted.
Modelling TRPV4 Skeletal Disorders Using Human IPSCs
Funder
National Health and Medical Research Council
Funding Amount
$1,171,187.00
Summary
Inherited skeletal disorders are a significant disease burden. Many gene mutations have been defined but we only have limited understanding about how they cause the disease. We will use patient skin cells and new in vitro re-programing technology to induce them to form cartilage cells to produce “disease in a dish” models of human skeletal disorders. These models will allow us to answer questions about how specific mutations cause disease and identify potential therapies
Improving Muscular Dystrophy By Targeting The ADAMTS5 Metalloproteinase
Funder
National Health and Medical Research Council
Funding Amount
$658,571.00
Summary
Muscular dystrophy is a devastating childhood disorder. There is no cure and no effective therapy to stop the disease progressing to early death. Our pilot data show that muscular dystrophy in a mouse model is dramatically improved when the Adamts5 gene is inactivated. ADAMTS5 is an enzyme that remodels the extracellular matrix around cells. This suggests that inhibiting ADAMTS5 may be a new way to treat muscular dystrophy. We will test this idea in mice with muscular dystrophy