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Defining The Function Of Apolipoprotein-D In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$457,231.00
Summary
Alzheimer's disease (AD) prevalence is rising and there is no curative treatment. Neurotoxic amyloid-beta peptide and concomitant lipid oxidation in the brain contribute to the cause of AD. We have identified a new pathway by which a protein called apoD may inhibit lipid oxidation in the AD brain. We will test the impact that changing apoD levels in neurons and in genetically modified mice has on neuron stress and AD-like characteristics. This may reveal new avenues to prevent or treat AD.
The ability to monitor one's cognitive performance deteriorates with normal ageing, and is particularly affected in a range of clinical conditions of older age, such as Parkinson's Disease, where it is a predictor of a poor prognostic outcome. This project aims to clarify the effects of age on cognitive and neural processes underlying performance monitoring, as an important first step to improving interventions for age-related impairments, including those accompanying neurodegenerative diseases.
Relationship Between Nigral Injury, Dopamine Handling And Dyskinesia In Parkinsonism
Funder
National Health and Medical Research Council
Funding Amount
$65,685.00
Summary
Parkinson's Disease is a disabling condition that results from loss of nerve cells (neurones) in the part of the brain known as the substantia nigra (SN). These neurones make dopamine. Symptoms become apparent when 80% of these neurones are gone, suggesting that compensation can occur in the brain. Dopamine can be replaced with the drug L-dopa. Unfortunately this benefit is not sustained and is frequently marred by the production of unpleasant writhing wriggling movements called dyskinesia. Thes ....Parkinson's Disease is a disabling condition that results from loss of nerve cells (neurones) in the part of the brain known as the substantia nigra (SN). These neurones make dopamine. Symptoms become apparent when 80% of these neurones are gone, suggesting that compensation can occur in the brain. Dopamine can be replaced with the drug L-dopa. Unfortunately this benefit is not sustained and is frequently marred by the production of unpleasant writhing wriggling movements called dyskinesia. These movements can also complicate the treatment for schizophrenia and other neurological conditions. The way the brain compensates for loss of SN neurones and why dyskinesia occur is unknown. However we present a hypothesis that the mechanisms for compensation also produce the dyskinesia. We have shown that an injury to the SN results in a compensatory response of vigorous sprouting of the surviving dopamine neurones. This sprouting may also explain why dyskinesias occur. The aim of this study is to establish whether the degree of compensatory response corresponds with the severity of dyskinesia and how this compensatory response can be modified or regulated.Read moreRead less
Control Of Mastication By Periodontal Mechanoreceptors In Man
Funder
National Health and Medical Research Council
Funding Amount
$169,990.00
Summary
Despite the importance in chewing and speech, very little is known regarding the fine control of jaw muscles. A thorough understanding of the control of the jaw muscles is at the base of improved diagnosis and treatment of many chewing disorders. For example: We still do not understand the causes of the jaw muscle-joint pain disorder (temporomandibular dysfunction) which accounts for about 5 % of total dental patients. The current treatments, including pain killers, night plates and massage cure ....Despite the importance in chewing and speech, very little is known regarding the fine control of jaw muscles. A thorough understanding of the control of the jaw muscles is at the base of improved diagnosis and treatment of many chewing disorders. For example: We still do not understand the causes of the jaw muscle-joint pain disorder (temporomandibular dysfunction) which accounts for about 5 % of total dental patients. The current treatments, including pain killers, night plates and massage cure only about half of all patients. Improved diagnosis and treatment techniques require more precise elaboration of the neural and muscular mechanisms of chewing. Why do the chewing forces in toothless individuals, despite well fitting dentures, fall to about 20 % of the value in teethed individuals? Do jaw muscles in these subjects weaken because they get less feedback from the receptors around the teeth? How does the chewing force automatically adjust to overcome sudden or gradual changes in the characteristics of foodstuff? Although bite to bite changes in the chewing force is observed in subjects with natural teeth, no such changes occur in toothless subjects or subjects chewing with implanted bridges. How do the receptors adjust the activation of jaw muscles so that bite force is applied in the right direction and right amount at each bite? The aim of this study is to define the importance of the periodontal mechanoreceptors (tiny nerve cells that are situated between the roots of the teeth and the jaw bone that signal bite force to the brain) in the control of jaw muscles. This study will, therefore, illustrate the importance of keeping the teeth and gums healthy for the development of strong, smooth and well-controlled chewing forces, and potentially create opportunities to improve chewing (and thereby quality of life) in toothless individuals or those experiencing other difficulties in chewing.Read moreRead less
Smoking Cessation And The Risk Of Cognitive Decline In Older Men
Funder
National Health and Medical Research Council
Funding Amount
$366,250.00
Summary
Dementia is one of the most relevant health issues at the turn of the millennium, and the identification of modifiable risk factors for Alzheimer's disease (AD) and vascular dementia (VD) is essential for the successful introduction of effective preventative strategies. The results of recent studies indicate that smoking increases the risk of cognitive decline, as well as the risk of AD and VD. These findings raise the possibility that cessation of smoking may reduce cognitive impairment in late ....Dementia is one of the most relevant health issues at the turn of the millennium, and the identification of modifiable risk factors for Alzheimer's disease (AD) and vascular dementia (VD) is essential for the successful introduction of effective preventative strategies. The results of recent studies indicate that smoking increases the risk of cognitive decline, as well as the risk of AD and VD. These findings raise the possibility that cessation of smoking may reduce cognitive impairment in later life and the risk of both AD and VD. Through the Perth Elderly Cohort Study (PECS), which involves a community-representative sample of 12203 men aged 65-83 years, we have a unique opportunity to investigate the effects of smoking and smoking cessation on the cognitive abilities of a large sample of older men at risk for cognitive decline. Clearly, evidence from an experimental study that smoking cessation is followed by a reduction in risk of cognitive decline would greatly strengthen the argument that smoking is truly a cause of cognitive impairment.Read moreRead less
Detection Of Alternative Lengthening Of Telomeres In The Mouse
Funder
National Health and Medical Research Council
Funding Amount
$471,000.00
Summary
In each cell, DNA is packaged into units called chromosomes, the ends of which (i.e., telomeres) become slightly shorter every time they are replicated during the production of new cells. Continued cell replication and hence continued telomere shortening eventually results in the inability of cells to replicate themselves any further. Normal cells have mechanisms to slow down, but not completely prevent telomere shortening. The development of a cancer depends on its cells being able to replicate ....In each cell, DNA is packaged into units called chromosomes, the ends of which (i.e., telomeres) become slightly shorter every time they are replicated during the production of new cells. Continued cell replication and hence continued telomere shortening eventually results in the inability of cells to replicate themselves any further. Normal cells have mechanisms to slow down, but not completely prevent telomere shortening. The development of a cancer depends on its cells being able to replicate themselves many times, and therefore they need to find a method to prevent their telomeres shortening. We discovered one such method, called Alternative Lengthening of Telomeres (ALT), that is used by some cancers. It has been shown in principle that cancer cells can be killed by disrupting their ability to prevent telomere shortening. Therefore, in another project we are developing methods needed to find drugs that inhibit ALT. In the meantime, we have found the first evidence that some normal cells have an ALT-like mechanism. Our speculation is that cancer cells are able to dysregulate and subvert this normal mechanism in order to prevent their telomeres from shortening. In this project, we will analyse the ALT-like mechanism in mice, to determine its characteristics, and to determine what tissues use it. This information will provide critically important insights into the ALT mechanism itself, and the likely side effects of drugs that inhibit ALT.Read moreRead less
Identifying Genetic Pathways Underlying The Development Of Distinct Neuronal Subtypes Among Midbrain Dopamine Neurons.
Funder
National Health and Medical Research Council
Funding Amount
$462,709.00
Summary
There is an urgent need in the field of Parkinson's disease (PD) research to develop new strategies aimed at halting progression of the disease (neuroprotection) and alleviaing the symptoms (restorative therapy). This project employs a novel and innovative design to identify genes expressed specifically by the cell type most effected in PD and therefore provide new genetic targets for neuroprotective and resorative therapy.
Regulation Of The Beta-secretase (BACE1) By Glycosaminoglycans
Funder
National Health and Medical Research Council
Funding Amount
$561,212.00
Summary
Alzheimer's disease is the leading cause of dementia in the elderly. Because of the prolonged institutionalisation of patients, it is a major health care burden. This project aims to develop novel drugs which can treat Alzheimer's disease by inhibiting production of the protein which causes the neurodegeneration.
Clinical And Biological Markers Of Disease Presentation And Progression In Early Frontotemporal Dementia
Funder
National Health and Medical Research Council
Funding Amount
$507,636.00
Summary
Frontotemporal dementia accounts for 12-20% of all dementia cases and is as common as Alzheimer's disease in the < 65 year olds. Our understanding of this disease remains limited. This project aims to better characterise the range and progression of deficits in early frontotemporal dementia using tests of brain function and magnetic resonance imaging. This will assist in better diagnosis of these patients and, ultimately, may be used to monitor the outcomes of therapeutic interventions.
The Role Of Down Syndrome Candidate Region 1 (DSCR1) In Neurotransmitter Release, Vesicle Recycling And Down Syndrome.
Funder
National Health and Medical Research Council
Funding Amount
$352,318.00
Summary
Individuals with Down syndrome (DS) have three copies of human chromosome 21 (HSA21), rather than the normal two. The symptoms observed in DS individuals are therefore due to the overexpression of HSA21 genes. Since all individuals with DS develop symptoms in the brain similar to those see in Alzheimer's disease (AD), there may be a common mechanism that can be traced to the extra gene dosage from HSA21. We are interested in one of these genes, Down syndrome candidate region 1 (Dscr1), which is ....Individuals with Down syndrome (DS) have three copies of human chromosome 21 (HSA21), rather than the normal two. The symptoms observed in DS individuals are therefore due to the overexpression of HSA21 genes. Since all individuals with DS develop symptoms in the brain similar to those see in Alzheimer's disease (AD), there may be a common mechanism that can be traced to the extra gene dosage from HSA21. We are interested in one of these genes, Down syndrome candidate region 1 (Dscr1), which is overexpressed in both DS and AD brains. We hypothesise that Dscr1 has a role in regulating exocytosis, a process in which chemical messengers are released from cells. Exocytosis is highly specialised in the brain where neurotransmitters are released from neuronal synapses in a process known as synaptic transmission. Reduced synaptic transmission is one of the earliest hallmark of DS and AD occurring long before the classical neurological traits of DS and AD such as plaque formation and dementia. We propose that alterations in Dscr1 expression are responsible for the reduced neuronal exocytosis observed in the early stages of DS and AD. We have generated mice in which Dscr1 expression is altered, as occurs in DS and AD brains, and our preliminary studies indicate that exocytosis is reduced in these mice. We now wish to find the intracellular changes responsible for regulating exocytosis when Dscr1 expression is altered. We also aim to compare this to exocytosis in classical DS mouse models which have an extra chromosome 21 and in similar DS mouse models which have normal levels of Dscr1. This project will uncover the currently unknown functions of Dscr1 in exocytosis in an animal model, allow us to gauge whether Dscr1 is solely responsible for altering exocytosis in DS amongst other HSA21 genes, enable us to better understand the mechanisms initiating DS and AD and possibly lead to new targets of early intervention in these diseases.Read moreRead less