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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.
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.
The Role Of A Presenilin 2 Truncation (PS2V) In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$552,741.00
Summary
The Presenilin and APP proteins are centrally important in inherited, early onset Alzheimer's disease. We have discovered that a shortened form of Presenilin protein, "PS2V", appears to increase specifically the rate at which the APP protein is cleaved to produce the "Amyloid beta" protein fragment that is found in Alzheimer's disease brains. This occurs when brain cells are under oxidative stress. Understanding this process will facilitate development of appropriate therapeutic strategies for t ....The Presenilin and APP proteins are centrally important in inherited, early onset Alzheimer's disease. We have discovered that a shortened form of Presenilin protein, "PS2V", appears to increase specifically the rate at which the APP protein is cleaved to produce the "Amyloid beta" protein fragment that is found in Alzheimer's disease brains. This occurs when brain cells are under oxidative stress. Understanding this process will facilitate development of appropriate therapeutic strategies for the disease.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.
Delineating The Mechanism Of Amyloid Beta Toxicity
Funder
National Health and Medical Research Council
Funding Amount
$565,242.00
Summary
Alzheimer’s disease and beta amyloid toxicity: Alzheimer’s disease (AD) is the most common form of dementia and is characterized by progressive memory loss, confusion, and cognitive deficits. In 2011, an estimated 269,000 Australians are currently living with dementia and without a significant medical breakthrough soon, it is anticipated that this will rise to about 981,000 by 2050
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 Role Of LIM Domain Kinase 1 In The Pathogenesis Of Alzheimer’s Disease
Funder
National Health and Medical Research Council
Funding Amount
$565,531.00
Summary
Alzheimer’s disease is characterized by progressive loss of cognition. Few Australians have remained untouched by the effects of Alzheimer’s disease in their families or social circles. Unfortunately, there is no cure and current therapies are limited to modest symptomatic relief. This project will explore the role of a protein that regulates the structural integrity of brain cells in disease, and test if targeting this protein could prevent disease progression.
Does IRAP Contribute To Alzheimer's Disease Pathology?
Funder
National Health and Medical Research Council
Funding Amount
$743,042.00
Summary
Alzheimer’s disease is a progressive brain disease which is results in memory loss and cell death. All currently prescribed drugs treat the memory loss but are unable to stop the deterioration of brain cells. We have developed a class of drugs that reverse memory loss. These drugs target a protein called insulin-regulated aminopeptidase, IRAP. We recently found that these drugs also reduce the disease pathology. This research proposal aims to investigate the role of IRAP in the initiation or pro ....Alzheimer’s disease is a progressive brain disease which is results in memory loss and cell death. All currently prescribed drugs treat the memory loss but are unable to stop the deterioration of brain cells. We have developed a class of drugs that reverse memory loss. These drugs target a protein called insulin-regulated aminopeptidase, IRAP. We recently found that these drugs also reduce the disease pathology. This research proposal aims to investigate the role of IRAP in the initiation or progression of Alzheimer’s disease pathology.Read moreRead less
Inflammation plays both protective and damaging roles in Alzheimer’s disease (AD), so to identify a long lasting and effective treatment, it is important that we better understand the underlying processes. Our studies implicate a cytokine called interleukin-18 (IL-18) as a factor that accelerates AD pathology. Here we propose to study the mechanisms by which this cytokine alters basic cell biological functions and how these changes affect AD pathogenesis.
Investigating Interleukin-37 As A Treatment And Biomarker For Alzheimer’s Disease
Funder
National Health and Medical Research Council
Funding Amount
$677,857.00
Summary
Alzheimer’s disease (AD) is the defining healthcare condition of our generation. Finding asymptomatic at risk individuals at preclinical stages will allow initiation of therapies that will either slow or, preferably, stop the progression of the disease. Herein, we will study a protein called interleukin-37 as an early biomarker and treatment for AD.