Vesicular Trafficking Pathways Underpinning Neuronal Secretion And Survival
Funder
National Health and Medical Research Council
Funding Amount
$697,209.00
Summary
Plethora of diseases of the nervous system are caused by defects in vesicular trafficking including neurodegenerative diseases such as Alzheimer’s disease. I will explore the mechanisms underpinning synaptic vesicular trafficking using novel super resolution techniques and reveal the how secretory vesicles traffic to the plasma membrane, undergo exocytosis, and recycle. I will also explain how in the crowded environment of the presynaptic terminals, retrograde cargoes are transported back to the ....Plethora of diseases of the nervous system are caused by defects in vesicular trafficking including neurodegenerative diseases such as Alzheimer’s disease. I will explore the mechanisms underpinning synaptic vesicular trafficking using novel super resolution techniques and reveal the how secretory vesicles traffic to the plasma membrane, undergo exocytosis, and recycle. I will also explain how in the crowded environment of the presynaptic terminals, retrograde cargoes are transported back to the cell body thereby carrying survival signals.Read moreRead less
Neuronal communication relies on the process of exocytosis by which neurons release a neurotransmitter. Exocytosis is critical for the simplest muscle movement to complex tasks such as learning and memory, and is altered in several neurodegenerative pathologies. We will investigate how the protein Munc18 controls exocytosis. This research will be important for understanding how neurons communicate in health and disease and will be relevant to other processes such as insulin release in diabetes.
Uncover How Myosin-6 Underpins The Ca2+-dependent Recruitment Of Secretory Vesicles To The Cortical Actin Network
Funder
National Health and Medical Research Council
Funding Amount
$559,295.00
Summary
Neuronal communication relies on the process of exocytosis by which neurons release a neurotransmitter. Exocytosis underpins processes such as the simplest muscle movement to complex tasks such as learning and memory, and is altered in several neurodegenerative pathologies. We will investigate how the protein Myosin-6 controls exocytosis. This research will be important for understanding how neurons communicate in health and disease and will be relevant to other processes such as insulin release ....Neuronal communication relies on the process of exocytosis by which neurons release a neurotransmitter. Exocytosis underpins processes such as the simplest muscle movement to complex tasks such as learning and memory, and is altered in several neurodegenerative pathologies. We will investigate how the protein Myosin-6 controls exocytosis. This research will be important for understanding how neurons communicate in health and disease and will be relevant to other processes such as insulin release in diabetes.Read moreRead less
Neuronal communication relies on the process of exocytosis by which neurons release a neurotransmitter. Exocytosis is critical for the simplest muscle movement to complex tasks such as learning and memory, and is altered in several neurodegenerative pathologies. We will investigate how the protein Munc18 controls exocytosis. This research will be important for understanding how neurons communicate in health and disease and will be relevant to other processes such as insulin release in diabetes.
TNF Traffic And Secretion In Astrocytes And Microglial Cells: Unveilling New Targets For Ischemic Stroke
Funder
National Health and Medical Research Council
Funding Amount
$585,070.00
Summary
Neurodegenerative disorders share a similar pathway to disastrous neurotoxicity, which occurs through the release of cytokines such as tumour necrosis factor-a (TNF) from glial cells. TNF controls inflammation but its excessive secretion in the brain is highly detrimental. The mechanism of TNF secretion is unknown but strategies aimed at reducing it have therapeutic potential. This grant proposes to study TNF discharge to find new ways to reduce secretion and confer protection in a stroke model.