Understanding The Pathophysiology Of Schizophrenia, Major Depressive Disorder And Bipolar Disorder As A Basis For Improving Treatments
Funder
National Health and Medical Research Council
Funding Amount
$804,106.00
Summary
The Applicant seeks to understand the causes of the schizophrenia, bipolar disorder and major depressive disorder, which affect over 20% of the Australian population. This research is important as drug design, based on chemical remodelling, has not significantly advanced initial breakthroughs in treating psychiatric disorders and there is now a widespread belief that new drugs will only come from understand their causes.
Understanding The Role Of Muscarinic Receptors In The Pathophysiology Of Depression And Bipolar Disorder
Funder
National Health and Medical Research Council
Funding Amount
$480,074.00
Summary
The causes of bipolar disorder and major depressive disorder, which effect many Australians, remain unknown. We have recently shown decreases in muscarinic receptors in the brain of people with bipolar disorder and major depressive disorder. Muscarinic receptors are important in maintaining the functions of the brain that seem to be affected in people with bipolar disorder and major depressive disorder. Here we seek to understand how changes in muscarinic receptors occur in both disorders.
Differential Changes In Cortical Tumour Necrosis Factor Signalling In Mood Disorders And Schizophrenia
Funder
National Health and Medical Research Council
Funding Amount
$642,078.00
Summary
Changes in inflammation-related pathways contribute to the symptoms of psychiatric disorders and tumour necrosis factor ? (TNF) is a protein central to regulating theses pathways. We have now shown that changes in pathways regulated by TNF are present in the brains of people with schizophrenia and mood disorders. This means that the symptoms experienced by those with the different disorders may be linked to differential changes in TNF-regulated pathways in the brain.
Molecular Mechanisms Underlying Recovery From General Anaesthesia
Funder
National Health and Medical Research Council
Funding Amount
$335,983.00
Summary
Even though general anaesthesia is an extremely common and safe procedure, doctors do not really know how it works. We have found that general anaesthetics might work in two steps, by first promoting natural sleep, and then by impairing communication between all nerve cells in the brain. It is this second step that makes surgery possible, but also makes recovery difficult – especially among patients with brain disorders. Understanding these mechanisms will promote better anaesthesia procedures.
Neurobiology Of Relaxin-3/RXFP3 Systems: Anatomical And Functional Studies In Transgenic Mice
Funder
National Health and Medical Research Council
Funding Amount
$94,242.00
Summary
Mental illness is an economic and health burden worldwide, with huge costs in medical spending, lost productivity, poor quality of life for sufferers and mortality. Relaxin-3 is a peptide that acts widely within neural circuits to modulate brain activity that is altered in conditions such as anxiety and mood/sleep disorders. Our research assessing the effect of genetic removal of relaxin-3 signaling on behaviour will add to our knowledge of brain function and improve mental health outcomes.
Utilising Functional Magnetic Imaging To Predict Pre-clinical Parkinson�s Disease In Patients With Idiopathic Rapid Eye Movement Sleep Behaviour Disorder
Funder
National Health and Medical Research Council
Funding Amount
$83,712.00
Summary
In an ageing Australian population a rise in the number of people with neurodegenerative conditions, such as Parkinson's Disease (PD) is inevitable. The ability to accurately identify those people who are destined to develop such diseases, might offer a mechanism by which such progression could be aborted. This project will seek to identify a reliable method whereby cases of PD could be detected several years before they can currently be diagnosed.
An inability to resist a temptation or repeated failures of self-regulation can lead to 'impulsive' and 'compulsive' behaviours that relate to a host of personal and social problems (eg., excessive eating, gambling, and substance use). Despite this, very little research has studied the neural and psychological underpinnings of these behaviours. My research will take advantage of recent innovations and approaches to fill this void and have implications for diagnosis and treatment.
Mimicking Slow Wave Sleep To Enhance Plasticity In The Elderly Human Brain
Funder
National Health and Medical Research Council
Funding Amount
$429,461.00
Summary
Cognitive and motor impairments associated with ageing have a major social and economic impact. This project will address a major driver of this decline. Brain functional decline is causally linked to poor sleep. Using non-invasive brain stimulation aspects of sleep important for maintaining cognitive and motor function will be mimicked, without the need for people to sleep. This will provide a new means to boost plasticity, and will assist in improving brain health throughout life.
Is The Eye A Window To The Brain In Sanfilippo Syndrome?
Funder
National Health and Medical Research Council
Funding Amount
$852,967.00
Summary
Study of the retina and optic nerve permits evaluation of central nervous system – these structures contain both neurons and glia and are outgrowths of the developing brain. Therefore, eye examination may allow us to study the brain and monitor brain disease and the effect of therapy. This project will determine whether brain disease in a childhood-onset disorder (Sanfilippo syndrome) and treatment of it, can be monitored in this way.
Sleep Disturbance And Cholinergic Degeneration In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$860,912.00
Summary
The largest class of drugs given to Alzheimer's disease patients aims to increase the function of cholinergic neurons that degenerate early in the disease. We will test whether disturbed sleep, which has been linked to Alzheimer's disease and cognitive decline are caused by neurodegeneration of these neurons, and whether early treatment can slow disease progression.