This project builds on findings of baseline data on the well-being and service usage of a small HACC sample population which demonstrated that carers of people with dementia (PWD) have high levels of stress and are caring for a very cognitively impaired group. In addition there was evidence that carers welcomed information and support which they were not accessing in a consistent way. This exciting research project involves a pilot randomised control trial of a new model of carer self help - Carers' Care - involving a DVD and a guidebook.
The aim of the program is to improve dementia knowledge among Tasmanian health care professionals and concurrently trial a dementia education program prior to a national rollout.
This study will develop, deliver, and evaluate the effectiveness of an education program designed to raise awareness and improve knowledge of dementia among health professionals and care staff.
This study aimed to improve knowledge in three primary areas of dementia care within the Tasmanian context.
Evaluating Aged Care Nurse Practitioners Models
An assessment and management service for people with memory & cognitive changes. This study will trial a nurse-led memory clinic in order to explore the clinics potential as a model of early primary health care for augmenting dementia diagnosis and therapeutic interventions.
To support the development of collaborative staff-family relationships in the residential aged care setting.
Understand quality of life (QoL) and related issues for people with dementia in residential aged care facilities (RACFs).
To support the transition of aged care facilities into the 21st Century we must create an environment that attracts leaders who will facilitate high performance cultures at a whole of organisation level. The Program has four projects:
May 2010 to Aug 2011
May 2010 to Aug 2011
Mar 2010 to Dec 2010
Jun 2009 to Dec 2010
Jun 2009 to Dec 2010
May 2009 to May 2010
Nov 2008 to Dec 2009
Jan 2008 to Dec 2011
Jan 2008 to Dec 2011
Sep 2007 to Dec 2009
May 2007 to May 2008
May 2006 to Apr 2008
Dec 2005 to Jun 2008
Aug 2005 to Jul 2006
May 2005 to Jun 2006
Apr 2005 to Mar 2006
Nov 2004 to Jun 2008
Jul 2004 to Jul 2005
Aug 2003 to Apr 2005
Mar 2002 to Apr 2003
Apr 2001 to Jun 2002
Apr 2001 to Dec 2002
Mild cognitive impairment (MCI) is a pre-dementia stage of subclinical cognitive decline. This study aims to develop accurate and reliable diagnostic criteria for MCI as a precursor to dementia.
The Tasmanian Healthy Brain Project (THBP) is a world-first prospective study examining the capacity of University level education to enhance cognitive reserve in older adults and subsequently reduce age-related cognitive decline and risk for neurodegenerative disease.
No previous programs.
A potential link has been drawn between anaesthesia in older people undergoing surgical procedures, and subsequent cognitive decline, which may increase the risk of dementia. We are investigating the role of anaesthetics in promoting the pathological changes associated with dementia.
Nerve processes are important for relaying information between nerve cells and when they dysfunction the nervous system fails to work properly. One reason that current therapeutics in neurodegenerative disease may not be successful, is that although they may protect the nerve cell they may not protect the nerve process from degenerating. We are using novel cell culture techniques to investigate the ways in which nerve processes degenerate and testing therapeutic agents that can protect them.
The aim of this project is to develop cell culture models that help us understand some of the complex cellular interactions that may underpin development of pathology in neurodegenerative disease.
The clinical onset of AD may be affected not only by an increase in the progression of pathological changes in the brain, but also by an individual’s cognitive reserve. This is evidenced by studies demonstrating that there is a large discrepancy between the amount of AD pathology and the clinical manifestations of dementia. It is believed that cognitive reserve may be increased by social and intellectual interactions. This is supported by epidemiological studies suggesting that lifetime environmental factors such as education can reduce the risk of dementia. The Wicking Dementia Research and Education Centre is exploring the association between later life education and ageing related cognitve decline and dementia in a world first prospective longitudinal study, The Tasmanian Healthy Brain Project (THBP).
Recently there has been a great increased understanding of the genetic basis of Frontotemporal dementia (FTD) and links have been drawn to the motor neuron disease amyotrophic lateral sclerosis (ALS). A number of proteins have been implicated either genetically or pathologically with these diseases, however the normal role of these proteins and relevance to disease is not clear.
This project has arisen from basic research conducted by Professor West and his group which has identified a family of proteins which protect the brain from injury and neurodegeneration. His group have developed synthetic analogues of these proteins which show promise in cell culture and animal models of Alzheimer’s disease. Understanding the pathway by which these agents work has generated new information on the mechanism by which neurons become dysfunctional, and eventually die, in neurodegeneration. His group is also investigating how this work might give rise to a non-invasive diagnostic test for Alzheimer’s. In a related project, he is investigating how the processes involved in degeneration of the brain compare to peripheral neuropathy, the degeneration of sensory nerves which occurs in diabetes and other conditions.
Alzheimer’s disease involves a loss of communication between the nerve cells of the brain. These nerve cells communicate vial long processes called axons. Axonal pathology is a key finding in Alzheimer’s disease and potential cause of cognitive decline. Our studies have shown that the protective myelin sheath surrounding nerve cell processes is lost in in close proximity to amyloid plaques and that this could contribute to axonal damage. We are investigating whether amyloid proteins, which are in high concentration in the brains of patients with AD, or other toxic chemicals, can contribute to the loss of myelin, oligodendrocytes, precursor cells or to the nerve process directly.
Repetitive transcranial magnetic stimulation (rTMS) is a new therapy which can modulate neuroplasticity in healthy and compromised brains. This translational project is investigating the neurophysiological and neurobiological mechanisms by which rTMS operates, both in humans and in animal models. Specifically, the project will:
- Investigate the effects of rTMS on corticospinal excitability (in humans) and axonal and/or dendritic synaptic structure (mouse).
- Investigate modulation of motor learning by rTMS and try to ascertain what synaptic changes are associated with this.
- Finally, the project will examine whether the changes in aims 1 and 2 are altered by normal ageing, and the associated changes in neuroplasticity.
To investigate inhibitory dysfunction, circuit disruption and excitability changes in ALS.
Traumatic brain injury is a leading cause of death and disability in individuals under the age of 45. Although the primary effects of TBI are well known, the secondary longer term effects may have an equally devastating burden on society. In this regard, TBI has been implicated as a risk factor in the development of Alzheimer’s disease. Currently the links between TBI and the subsequent development of AD pathology are unclear, however determining these links could lead to the development of therapeutic strategies to be used either immediately following, or in the years after, a traumatic injury.
This project investigates how changes in sensory input trigger downstream neuronal reorganisation that ultimately modulates the production and aggregation of Aβ peptides. It builds on our recent exciting data showing that long-term denervation of the olfactory bulb leads to decreased Aß aggregation in the bulb and cerebral cortex including the hippocampus, in a familial AD transgenic model (APP/PS1 mice).
2009 to 2010
2009 to 2012
2008 to 2011
2007 to 2008
2007 to 2008
2007 to 2010
2005 to 2006
2003 to 2006