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A New Function For An Old Enzyme: Src Protein Kinase Directs Excitotoxic Neuronal Death In Stroke
Funder
National Health and Medical Research Council
Funding Amount
$513,975.00
Summary
In our previous investigation of how brain cells die in patients suffering from stroke, we found that stroke causes aberrant activation of an enzyme called Src in the affected brain cells. Furthermore, this aberrantly activated Src directs the brain cells to undergo cell death. Our proposal, which aims to decipher this neurotoxic mechanism of the aberrantly activated Src will benefit development of new therapeutic strategies to reduce brain damage in stroke patients.
IS THERE A ROLE FOR ENDOPLASMIC RETICULUM STRESS IN THE PATHOGENESIS OF ALS?
Funder
National Health and Medical Research Council
Funding Amount
$535,710.00
Summary
Motor neuron disease (MND) is a devastating and rapidly progressing adult onset disease; most patients die 2-5 years after diagnosis. MND is characterized by the death of specific cells, called 'motor neurons' within the nervous system. Unfortunatley, MND currently has an unknown cause and no effective treatment. This proposal aims to study the mechanisms that trigger degeneration of motor neurons in MND. Some forms of MND are inherited and linked to mutations in a protein called SOD1, but how t ....Motor neuron disease (MND) is a devastating and rapidly progressing adult onset disease; most patients die 2-5 years after diagnosis. MND is characterized by the death of specific cells, called 'motor neurons' within the nervous system. Unfortunatley, MND currently has an unknown cause and no effective treatment. This proposal aims to study the mechanisms that trigger degeneration of motor neurons in MND. Some forms of MND are inherited and linked to mutations in a protein called SOD1, but how the mutations lead to cell death is unclear. However, SOD1 mutants are known to clump together in large aggregates and this is linked to toxicity. In a previous study, we found that normally SOD1 is secreted from the cell where it can protect the motor neuron from oxidative damage. However SOD1 mutants are not secreted as well as the normal protein, leaving the cell vulnerable to damage. In addition, the compartment of the cell responsible for secretion,the 'endoplasmic reticulum' (ER), is under stress due to secretory dysfunction of mutant SOD1. Our data suggest that this ER stress leads to the activation of 'cell suicide' pathways, leading to death of the motor neuron. However, very little is known about how molecular events in the ER lead to cell death in MND. This proposal will examine these processes in detail. In other studies, we found that a molecule called 'PDI' inhibits mutant SOD1 from aggregation and is made in large quantities in our laboratory models of MND. This proposal will determine if PDI is potentially a new therapeutic target for MND due its ability to protect the cell from the toxic effects of SOD1 aggregation. Our findings are both novel and exciting and propose previously unexplored mechanisms of disease and new theraputic targets. Once we understand the basic mechanisms occuring in the motor neuron, which we can design specific therapies to halt the progression of the disease and prolong the life of human MND patients.Read moreRead less
Protein Phosphatase 2A Methylation: Regulation And Functional Significance For Tauopathies
Funder
National Health and Medical Research Council
Funding Amount
$470,713.00
Summary
Clinical studies have revealed that low blood levels of the vitamin folate are a risk factor for cognitive impairment, depression and dementia, which are prevalent in the elderly. Deregulation of the protein tau is a key event in Alzheimer’s disease pathogenesis. This project will utilize cell culture and aged mouse models to determine how alterations in folate status and deregulation of protein phosphatase 2A affect the regulation of tau and other key brain processes that become altered in Alzh ....Clinical studies have revealed that low blood levels of the vitamin folate are a risk factor for cognitive impairment, depression and dementia, which are prevalent in the elderly. Deregulation of the protein tau is a key event in Alzheimer’s disease pathogenesis. This project will utilize cell culture and aged mouse models to determine how alterations in folate status and deregulation of protein phosphatase 2A affect the regulation of tau and other key brain processes that become altered in Alzheimer’s disease.Read moreRead less
Mitochondria: Molecular And Cellular Insights Into Their Diverse Contributions To Neuronal Injury
Funder
National Health and Medical Research Council
Funding Amount
$747,927.00
Summary
Mitochondria are components of cells normally providing energy for essential functions and in the energy demanding brain, under stress conditions, mitochondria acts as controllers of cellular decision-making processes leading to neuronal death. Our goal is to understand mitochondrial mechanisms determining how neurones die after various stresses and injury. Using pathological insults relevant to neurological conditions, we shall analyse death molecules and how neurones adapt when threatened.
In Parkinson's disease only specific brain cells die, these cells are unusual in that they contain a dark coloured pigment called neuromelanin. The presence of this pigment is thought to play a role in the death of these cells. Evidence from many different diseases has demonstrated that a type of cell damage called oxidative damage is caused by an increase in tissue iron levels. Iron levels are increased in the brains of persons who have died with Parkinson's disease but only in the part of the ....In Parkinson's disease only specific brain cells die, these cells are unusual in that they contain a dark coloured pigment called neuromelanin. The presence of this pigment is thought to play a role in the death of these cells. Evidence from many different diseases has demonstrated that a type of cell damage called oxidative damage is caused by an increase in tissue iron levels. Iron levels are increased in the brains of persons who have died with Parkinson's disease but only in the part of the brain which contains neuromelanin. This increase in iron is thought to lead to oxidative damage and thus cell death in Parkinson's disease. Why iron should be increased specifically in this part of the brain is unknown but it has been shown that neuromelanin binds tissue iron and that the interaction between iron and neuromelanin can result in tissue damage. These events are suggested to underlie the specific vulnerability of the neuromelanin-containing cells in Parkinson's disease. However as yet very little is known about this pigment or how it interacts with iron. This research investigates neuromelanin in the normal brain and in the brain of persons who have died with Parkinson's disease. The project aims to demonstrate how neuromelanin interacts with iron and how neuromelanin, both in the presence and absence of iron, can influence oxidative cell damage. The use of human neuromelanin makes this research unique and it will provide important and novel information regarding the role of this pigment in the aetiology of this devastating disease.Read moreRead less
Targetting Nogo A As A Means To Promote CNS Axonal Regrowth
Funder
National Health and Medical Research Council
Funding Amount
$325,911.00
Summary
Unlike the peripheral nervous system, regenerative nerve fiber growth and structural plasticity are limited in the adult mammalian central nervous system (CNS), following injury. Although lesioned axons can sprout spontaneously, this regeneration attempt is transitory and no significant re-growth occurs over long distances. Consequently, injury to the CNS often leads to permanent disability. In many cases, it has been shown that it is not the absence of growth-promoting molecules in the CNS but ....Unlike the peripheral nervous system, regenerative nerve fiber growth and structural plasticity are limited in the adult mammalian central nervous system (CNS), following injury. Although lesioned axons can sprout spontaneously, this regeneration attempt is transitory and no significant re-growth occurs over long distances. Consequently, injury to the CNS often leads to permanent disability. In many cases, it has been shown that it is not the absence of growth-promoting molecules in the CNS but rather the presence of axon outgrowth inhibitors, including components of both CNS myelin and astroglial scars that limit regeneration. Given that axonal injury is an important pathological determinant of permanent disability in multiple sclerosis (MS), we have recently investigated the role of the CNS neurite outgrowth inhibitor, Nogo A in the development of a chronic form of murine MS-like disease. We showed that targeting Nogo A by active and passive immunization blunts clinical signs, demyelination and axonal damage associated with this model of MS. These results identify Nogo A as an important determinant of the development of autoimmune-mediated demyelination and suggest that its blockage may help to maintain and-or to restore the neuronal integrity of the CNS after autoimmune insult in disease such as MS. The principal goal of this application is to study the mechanism by which blockade of Nogo A improves clinical outcome in disease like MS and to determine whether neurite sprouting accounts for such an improvement. Targeting Nogo A and-or its receptor, has the potential to not only regulate-modulate the process of autoimmune mediated demyelination but could lead to the first therapy ever offered to patients that helps damaged nerves regenerate after axonal injury following neurodegeneration due to insult or disease.Read moreRead less