A Multi-cohort Investigation Of The Effects Of BDNF Val66Met On Tau, Neurodegeneration And Cognition In Preclinical Alzheimer’s Disease
Funder
National Health and Medical Research Council
Funding Amount
$325,758.00
Summary
There are currently no disease modifying therapies for Alzheimer’s disease. We will elucidate the role of a genetic polymorphism that has previously been shown to exert neuroprotective effects on memory decline and brain volume loss associated with Alzheimer’s disease. By studying the role of this gene in multiple cohorts of individuals with varying degrees of Alzheimer’s disease risk, this study has high potential to uncover novel disease-modifying strategies for the treatment of the disease.
Seizures appear unpredictable and greatly affect the quality of all aspects of life for patients with epilepsy and their carers. New advances in complex systems theory suggest that transitions from normal brain activity to seizures are preceded by measurable changes in the brain’s responses to stimuli, known as critical slowing. Measurement of critical slowing will enable prediction of seizures, providing a warning system, and possibly an opportunity to deliver preventative therapies.
Mild Traumatic Brain Injuries And Neurodegenerative Disease
Funder
National Health and Medical Research Council
Funding Amount
$928,690.00
Summary
Repeated mild traumatic brain injuries (RmTBIs) have been linked to the development of neurodegenerative conditions. However, whether RmTBIs cause neurodegenerative disease, and the factors involved, requires further research. Using an innovative rat model, this project will examine whether RmTBIs cause long-term neurological changes resembling neurodegenerative disease. This cutting-edge project is highly relevant to human patients and will improve our understanding of these common injuries.
The Role Of Central Haemodynamics In Type 2 Diabetes Mellitus-related Brain Disease
Funder
National Health and Medical Research Council
Funding Amount
$899,704.00
Summary
Type 2 Diabetes Mellitus is associated with stiffening of major blood vessels which may allow the transmission of harmful pressure to the small vessels of the brain. This may in turn be responsible for damage to brain cells and a greater risk of dementia. This study will use state-of-the art techniques to test this theory. If true, it may open opportunities to reduce the risk of brain disease in diabetes by using therapies to reduce arterial stiffening.
Restoration Of Cognitive Deficits Induced By Diabetes Through The Modulation Of Cerebrovascular Integrity
Funder
National Health and Medical Research Council
Funding Amount
$261,251.00
Summary
Diabetes is a known risk factor for the development of dementia. However the details of this association have not been known. Recent evidence consistently shows that the integrity of blood vessels in the brain may be central to the onset of dementia, and consistently, damaged brain blood vessels are often reported in diabetic patients and animal models. This project is the first to target in restoring the integrity of those brain blood vessels in order to reverse diabetes-associated dementia.
Cannabidiol (CBD): A Novel Therapeutic For Alzheimer's Disease.
Funder
National Health and Medical Research Council
Funding Amount
$775,005.00
Summary
Current drugs do not stop or reverse the progression of Alzheimer’s disease (AD). Also, brains of AD patients show a number of biological changes and effective drugs should target those together. Cannabidiol (CBD) has such abilities when tested in AD cell models. We found that CBD can also prevent and reverse memory deficits in AD mice. We propose to provide convincing preclinical evidence for the benefits of CBD for human AD therapy and to define mechanisms involved.
Mechanisms Of PTEN Regulation By Ndfip1 And Their Biological Consequences For Neuron Survival During Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$686,640.00
Summary
We have discovered a new protein (Ndfip1) that protects brain cells from death after brain injury from trauma and stroke. We will investigate why this protein is activated only in some, but not in other, brain cells after injury. In this application, we will study the mechanisms behind neuron protection, and use this information to explore how to increase the number of brain cells activating Ndfip1.
This study investigates how much an individual's genes and environment account for the wide variation in brain structure and function. Using brain imaging we examine in what way the connectivity of the brain of identical and non-identical twins is the same or different from that of their co-twin, and carry out analysis of their DNA to identify some of the genes involved. This will provide fundamental information on genetic mechanisms influencing variation in brain structure and function.
Blood-Brain Barrier Penetrating Antisense Therapy For Spinal Muscular Atrophy
Funder
National Health and Medical Research Council
Funding Amount
$635,005.00
Summary
Spinal muscular atrophy (SMA) is a genetic disease caused by the deficiency of a protein known as survival motor neuron.This results in the degeneration of motor neurons (nerve cells controlling muscles) leading to progressive muscle weakness, paralysis, and eventual death. Currently, there is no known cure for SMA. The aim of proposed research is to develop gene-modifying molecules that prevent degeneration of motor neuron and extend the life-span of mice as a potential therapy for SMA.
Exploring Scanning Ultrasound (SUS), A Novel Method To Treat And Prevent Neurodegenerative Disease
Funder
National Health and Medical Research Council
Funding Amount
$765,708.00
Summary
We developed a novel scanning ultrasound (SUS) protocol that clears toxic protein aggregates and restores memory function in mouse models of Alzheimer's disease (AD), without the need for therapeutic agents. Here we aim to determine whether SUS has preventative potential, whether there are synergistic effects, and whether a therapeutic antibody combined with SUS leads to an enhanced therapeutic outcome. Together this will guide the development of an ultrasound therapy in AD patients.