Neurophysiological Basis For Sensorimotor Interventions In Rehabilitation After Stroke
Funder
National Health and Medical Research Council
Funding Amount
$332,036.00
Summary
Stroke is estimated to cost the Australian government almost $2 billion annually, and is the most common cause of death after heart disease and cancer and one of the largest single causes of long-term disability. Of people who survive a stroke, a large number have some degree of residual motor dysfunction on one side of the body. Motor rehabilitation programmes are generally considered to enhance the recovery of motor function and to reduce the degree of long-term disability. However the rationa ....Stroke is estimated to cost the Australian government almost $2 billion annually, and is the most common cause of death after heart disease and cancer and one of the largest single causes of long-term disability. Of people who survive a stroke, a large number have some degree of residual motor dysfunction on one side of the body. Motor rehabilitation programmes are generally considered to enhance the recovery of motor function and to reduce the degree of long-term disability. However the rationale for the design of effective rehabilitation programmes is largely empirical, and there is uncertainty regarding the efficacy and cost-effectiveness of currently used therapies. The empirical nature of stroke rehabilitation has resulted in a diversity of techniques, many of which were pioneered 30-40 years ago, and which are generally aimed at enhancing brain plasticity as a means to facilitate motor recovery. However, despite the belief that brain plasticity is a key to recovery, it is still not known how best to develop this potential for reorganisation into practical interventions that could be introduced in stroke rehabilitation. The aim of the present study is to investigate the physiological bases for the action of commonly used sensorimotor rehabilitation strategies and identify those strategies which are most effective in bringing about corticomotor reorganisation, in the belief that such reorganisation is fundamental to motor recovery. Specifically we will investigate the changes in the organisation of the cortical projection to muscles of the upper limb as a result of passive movement, resisted and non-resisted movement, increased functional motor use and visuomotor training programmes. It is anticipated that the study will lead to a better understanding of the physiological basis for therapeutic interventions after stroke and will allow a more rational approach to the design of effective rehabilitation programmes for stroke patients.Read moreRead less
Novel Approaches To Nanomedicines For Future Therapies
Funder
National Health and Medical Research Council
Funding Amount
$2,414,215.00
Summary
Nanomedicines have the potential to transform healthcare by targeting significant health issues such as Alzheimer’s, diabetes and Parkinson’s diseases that have mainly eluded successful therapeutic solutions. In addition, nanotechnology has the potential to significantly improve the treatment of chronic pain by repurposing analgesic medications for improved effectiveness without significant side effects. I will target these two areas of research during the next five years.
Functional Assessment Of Bioenergetic Defects In Hereditary Spastic Paraplegia
Funder
National Health and Medical Research Council
Funding Amount
$113,322.00
Summary
Hereditary spastic paraplegia (HSP) is a degenerative, hereditary disorder which affects the legs. Currently there are no treatments that target the disease process. We seek to identify the genes responsible for this condition in a group of Australian patients. Cell samples obtained from these patients will be tested for energy defects. We hope to improve our understanding of the underlying disease processes in order to find new ways to prevent, treat and cure this condition.
L1 Retrotransposition: The Missing Link Between Genetics And Environmental Factors In Parkinson's Disease ?
Funder
National Health and Medical Research Council
Funding Amount
$604,644.00
Summary
The study proposed here focuses on understanding the role of specific mobile DNA sequences in the interaction between environmental and genetic risk factors causing Parkinson’s disease (PD) leading to dementia. The project proposes identification of mobile DNA induced mutations in post-mortem human PD patient brain samples. The significance and mechanisms of mobile DNA induced mutations will be then tested in a PD mouse model.
Non-HFE Haemochromatosis In Australia: Natural History And Molecular Characterisation
Funder
National Health and Medical Research Council
Funding Amount
$179,948.00
Summary
Hereditary haemochromatosis (HH) is a disorder characterised by excessive iron absorption and build up of iron in body organs such as the liver. The excess iron can be toxic and cause disease. Most HH is caused by mutations in the HFE gene. Other forms are caused by mutations in other genes. This project will characterise a new form of HH that is unrelated to any of the previously known genes. The project aims to find the gene for this new condition by genetic analysis in a large family.
Harnessing The Human Postmortem Brain To Elucidate Changes In FK506 Binding Protein (FKBP5) In The Neuropathology Of Severe Psychiatric Disorders
Funder
National Health and Medical Research Council
Funding Amount
$392,052.00
Summary
The postmortem human brain is a unique source to search for the pathological basis of severe psychiatric disorders including major depression, bipolar disorder and schizophrenia. Postmortem tissues are however being underutilised. This project will apply a selection of powerful biochemical measuring techniques to postmortem human brain tissues to uncover the molecular pathways of severe psychiatric disorders, which is knowledge that can lead to better treatments, preventions and cures.
Defining The Changes In Cell Biology Caused By PRESENILIN Truncations Associated With Different Diseases
Funder
National Health and Medical Research Council
Funding Amount
$622,886.00
Summary
Truncations of the PRESENILIN genes in humans can cause two very different diseases: inherited, early onset Alzheimer’s disease (familial Alzheimer's disease) and a skin disease named inherited Acne Inversa. One truncation is also involved in the non-inherited, late onset form of Alzheimer’s disease. Why do these different truncations produce different diseases? Investigating this question will teach us more about the molecular bases of these different diseases. This understanding will be requir ....Truncations of the PRESENILIN genes in humans can cause two very different diseases: inherited, early onset Alzheimer’s disease (familial Alzheimer's disease) and a skin disease named inherited Acne Inversa. One truncation is also involved in the non-inherited, late onset form of Alzheimer’s disease. Why do these different truncations produce different diseases? Investigating this question will teach us more about the molecular bases of these different diseases. This understanding will be required for the development of treatments.Read moreRead less
I am a molecular biologist and my research is focussed on the importance of epigenetics in early development and disease, especially in cancer. My research to date has resulted in many ground-breaking discoveries relating to DNA methylation patterns, that