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Blood Protein Biomarkers For Frontotemporal Lobar Degeneration
Funder
National Health and Medical Research Council
Funding Amount
$184,305.00
Summary
This project will assess blood proteins as biomarkers for different pathogenic forms of frontotemporal dementia (FTD), one of the major neurodegenerative dementias with a very rapid disease progression (mean survival 3 years). At present, it is not possible to predict which pathological variant is present in any given patient. We plan to develop blood protein biomarker assays capable of diagnosing the pathology in vivo.
Neuroprotective Functions Of Autophagy Regulators In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$434,644.00
Summary
The accumulation of the beta amyloid protein has a central role in AD and enhancing its removal improves memory loss in animal AD models. This project builds on my recent finding of regulators of a cell housekeeping system, “autophagy” which accelerate removal of beta amyloid in cells. This study will advance knowledge into the protective functions of the autophagy regulators in reducing AD symptoms. Findings from this work might provide the basis for developing effective anti-AD therapeutics.
A Role Of Sortilin In The Development Of Alzheimer's Disease
Funder
National Health and Medical Research Council
Summary
Alzheimer’s disease is the most common form of dementia and is caused by both environmental and genetic variations. With aging, a toxic peptide accumulates in the brain and causes loss of memory and cell death. This study aims to elucidate how the toxic peptide is generated and how its precursor trafficks within nerve cells.
Sortilin Forms A Complex With APP And BACE To Regulate Abeta Production
Funder
National Health and Medical Research Council
Funding Amount
$208,910.00
Summary
Alzheimer's disease is a neurodegenerative disorder which is highly prevalent in aging population. Amyloid beta is a toxic peptide derived from a metabolic processing of its precursor amyloid precursor protein (APP). This project will examine how a novel protein called sortilin interacts with APP and its processing enzyme and how the toxic peptide is produced. Understanding the trafficking of APP and beta-secretase ?BACE? regulated by sortilin may help understanding how Alzheimer's disease is de ....Alzheimer's disease is a neurodegenerative disorder which is highly prevalent in aging population. Amyloid beta is a toxic peptide derived from a metabolic processing of its precursor amyloid precursor protein (APP). This project will examine how a novel protein called sortilin interacts with APP and its processing enzyme and how the toxic peptide is produced. Understanding the trafficking of APP and beta-secretase ?BACE? regulated by sortilin may help understanding how Alzheimer's disease is developed.Read moreRead less
Use Of The P75NTR Extracellular Domain As A Therapeutic Target For The Treatment Of Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$733,633.00
Summary
AlzheimerÍs disease is the most common form of dementia and is caused by both environmental and genetic variations. With aging, a toxic peptide accumulates in the brain and causes loss of memory and cell death. This study aims to elucidate how the toxic peptide is generated and how to remove it in order to prevent and treat the disease.
IRON EXPORT PROTEIN FAILURE IN PARKINSONISM AND DEMENTIA
Funder
National Health and Medical Research Council
Funding Amount
$843,352.00
Summary
We recently discovered a novel relationship between the Alzheimer’s amyloid precursor protein (APP) and tau, and that both proteins play a role in regulating iron levels in the brain. We predict that a loss or multiple failures in these iron-regulating systems could foster a toxic iron accumulation in brain, leading to the development of diseases with dementia such as Alzheimer’s and Parkinson’s diseases. We hope to gain a better understanding of their mechanism of action and propose that this p ....We recently discovered a novel relationship between the Alzheimer’s amyloid precursor protein (APP) and tau, and that both proteins play a role in regulating iron levels in the brain. We predict that a loss or multiple failures in these iron-regulating systems could foster a toxic iron accumulation in brain, leading to the development of diseases with dementia such as Alzheimer’s and Parkinson’s diseases. We hope to gain a better understanding of their mechanism of action and propose that this pathway is a target for therapeutic intervention.Read moreRead less
The Pathway Linking Tau And APP In Neurodegeneration
Funder
National Health and Medical Research Council
Funding Amount
$312,085.00
Summary
Recently I co-discovered a novel relationship between the AlzheimerÍs amyloid precursor protein and tau, both of which play a role in regulating neuronal iron levels. I predict that multiple failures in iron-regulating systems could foster a toxic iron accumulation in brain, leading to the development of neurodegenerative diseases. I hope to gain a better understanding of their mechanism of action and propose that this pathway is a target for therapeutic intervention.
PYROXD1 - A Novel Myopathy Disease Gene Identifies A Redox Pathway Essential For Life
Funder
National Health and Medical Research Council
Funding Amount
$1,247,992.00
Summary
An Australian family with a rare myopathy has led to the discovery of a new gene called PYROXD1; a gene that all cells need to survive. PYROXD1 plays a critical role in protecting cells from oxidative stress. We are using patient samples and mouse models to find out what PYROXD1 does that is vital for cell and animal life. We will test whether redox therapies developed for neurodegenerative disorders might help patients with rare neuromuscular disorders, for whom there are no treatment options.
The Role Of Beta-Amyloid Precursor Protein And Tau In The Regulation Of Neuronal Iron
Funder
National Health and Medical Research Council
Funding Amount
$650,226.00
Summary
We have recently discovered a novel relationship between amyloid precursor protein (APP) and tau in regulating neuronal iron balance. This project will establish how tau aids APP transport to the cell surface where it assists cellular iron release. A commonality in some neurodegenerative diseases are disruptions in either proteinsÍ function and iron-related excitotoxicity. Understanding the iron role of APP and tau will lead to a therapeutic mechanism of action and better future drug design.
Investigating Drug Treatments For A Machado Joseph Disease Using Transgenic Zebrafish
Funder
National Health and Medical Research Council
Funding Amount
$443,425.00
Summary
Machado Joseph disease (MJD) is a hereditary neurodegenerative disease that causes problems with a patient’s co-ordination and movement, leading to paralysis and death. Although the disease affects patients throughout the world, it is most common within Aboriginal communities of Arnhem Land in the Northern Territory. This project seeks to identify a drug treatment for the disease by examining the effect of relevant drugs on zebrafish genetically modified to have the human gene that causes MJD.