Neuroprotective Functions Of Autophagy Regulators In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$434,644.00
Summary
The accumulation of the beta amyloid protein has a central role in AD and enhancing its removal improves memory loss in animal AD models. This project builds on my recent finding of regulators of a cell housekeeping system, “autophagy” which accelerate removal of beta amyloid in cells. This study will advance knowledge into the protective functions of the autophagy regulators in reducing AD symptoms. Findings from this work might provide the basis for developing effective anti-AD therapeutics.
Dementia is the third leading cause of death in Australia and the single greatest cause of disability in the elderly. Current therapies for Alzheimer’s disease (AD), the most common form of dementia, are inadequate and fundamentally new treatment approaches are required. The aim of this proposal is to develop novel drug candidates for the treatment and prevention of AD and other neurodegenerative disorders by targeting a class of cell-surface receptors called G protein-coupled receptors (GPCRs).
Alzheimer’s disease (AD), is the most common form of dementia, accounting for between 50-70% of all cases. There is general agreement that current treatments for AD/dementia are inadequate so new treatment strategies are desperately needed. I am addressing these challenges by developing new technologies to generate next generation treatments for AD.