Nerve cells communicate with each other through nerve processes or neurites. The dysfunction of neurites results in the clinical symptoms of dementia such as cognitive decline. Currently we cannot directly monitor degeneration of neurites in the living brain and therefore it is difficult to determine whether therapeutic agents are protective. My goal is to develop a detection system in the blood that will allow us to monitor these changes during disease progression and therapeutic intervention.
There are escalating numbers of Alzheimer�s disease sufferers. This Project aims to provide a better understanding of the fundamental process underlying the damage to brain circuitry in this condition. This proposal may provide key information regarding the relationship between the major pathological changes of Alzheimer�s disease, identifying the cellular mechanisms that are crucial to this process, and providing new avenues for therapeutic agents targeted at the earliest stage of AD.
Preclinical Evaluation Of The Novel Therapeutic Compound APP96-110 In An Ovine Model Of Traumatic Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$874,734.00
Summary
Traumatic brain injury (TBI) is a significant cause of death and disability, and yet there are currently no effective treatments to improve outcome following such an insult. Our laboratory has developed a novel therapeutic compound, by identifying an endogenous neuroprotective molecule, in the amyloid precursor protein and then identifying the active site and modifying it to improve its efficacy. We will be testing this compound in our sheep model of TBI.
Validating Novel Serum Markers Of Neurodegeneration In Multiple Sclerosis Patients.
Funder
National Health and Medical Research Council
Funding Amount
$516,304.00
Summary
In multiple sclerosis (MS), permanent disability occurs when brain cells known as neurons are damaged following an immune attack. Current treatments reduce the number and severity of immune attacks, but they do not prevent neuron damage or permanent disability in many patients. There is currently no direct way to measure neuron damage in humans, so it is difficult to develop new drugs to prevent it. To address this need, we will trial a new blood test for measuring neuron damage in MS patients.
AUSSPRINT:Australian Study Of The Effects Of Strict Potassium Restriction On Neuropathy In Chronic Kidney Disease.
Funder
National Health and Medical Research Council
Funding Amount
$252,653.00
Summary
Patients with chronic kidney disease, when compared to healthy controls, are weaker, less active and have reduced exercise capacity. These physical limitations have in turn been linked to low quality of life and higher mortality rates. Studies have shown that high blood levels of potassium may cause nerve damage in chronic kidney disease patients.This study explores the benefits of strict potassium restriction as a means of reducing neuropathy rates in patients with chronic kidney disease.