The Role Of TGFB1 In The Pathophysiology Of Late Stage Schizophrenia
Funder
National Health and Medical Research Council
Funding Amount
$612,961.00
Summary
Schizophrenia is triggered in people with a genetic predisposition by as yet unknown environmental factors. Having shown that changes in gene expression in the brains of people with schizophrenia vary as the disease progresses, this application seeks to understand the changes in a pathway regulated by transforming growth factor ?1 that occur late in the progression of the illness. Understanding the changes in this important pathway could affect how people with schizophrenia are treated as their ....Schizophrenia is triggered in people with a genetic predisposition by as yet unknown environmental factors. Having shown that changes in gene expression in the brains of people with schizophrenia vary as the disease progresses, this application seeks to understand the changes in a pathway regulated by transforming growth factor ?1 that occur late in the progression of the illness. Understanding the changes in this important pathway could affect how people with schizophrenia are treated as their disorder progresses.Read moreRead less
Lysosomal Dysfunction As An Inhibitor Of Vitamin B12 Utilisation In Neurodegenerative Diseases
Funder
National Health and Medical Research Council
Funding Amount
$554,901.00
Summary
Vitamin B12 is required for red blood cell formation, DNA synthesis and normal neurological function. B12 deficiency contributes to age-related cognitive decline and Alzheimer’s disease. This research will provide important new information regarding the ageing process and the impact that brain changes associated with ageing and Alzheimer's disease have on B12 metabolism. It will provide important information related to the therapeutic potential of B12.
The research outlined in this application seeks to examine the role of calcium in the pathogenesis of AD. It will examine the hypothesis that the build-up of a protein known as the Abeta causes an increase in levels of calcium in nerve cells of the brain. This increase in calcium may trigger nerve cell damage and dementia. The ultimate aim of the research is to identify new targets for drug development in Alzheimer's disease.
Defining The Mechanisms By Which ABCA7 And ApoE Control Alzheimer's Disease Risk. Functional Characterisation Of New Therapeutic Targets For Dementia Prevention And Treatment.
Funder
National Health and Medical Research Council
Funding Amount
$687,975.00
Summary
Alzheimer’s disease (AD) is the major cause of dementia and is currently without a curative treatment. An understanding of the pathways that lead to AD is urgently required to develop approaches for treatments. We have discovered new pathways by which proteins called ApoE and ABCA7 control AD. We now aim to define precisely how these proteins work in the brain and use this information to develop therapeutic approaches to treat AD in humans.
Isoform-dependent ApoE Processing By Human Induced Pluripotent Stem Cells. A Novel Pathway Linking APOE Genotype And Alzheimer’s Disease Risk.
Funder
National Health and Medical Research Council
Funding Amount
$429,495.00
Summary
We recently discovered that a protein called apoE is cleaved in the brain to generate a small fragment that may have neuroprotective properties. We also discovered that human induced pluripotent stem cell (iPSC)-derived neurons produce apoE fragments identical to those in the brain. We will now characterise iPSC apoE and assess its neuroprotective properties. This will resolve the basis for the association of apoE with AD risk and potentially provide a new target for AD treatment.
Targeting Post-synaptic Tau To Treat Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$1,686,311.00
Summary
We have previously identified post-synaptic tau as being critical in mediating toxicity in Alzheimer's disease brains. This project aims at understanding the exact underlying molecular mechanisms and, more importantly, developing novel drugs to block early toxicity that initiates cascades that eventually lead to brain atrophy and dementia. To achieve this aim, this project will generate and utilize models of Alzheimer's disease in combination with a broad range of latest analytical tools.