The mechanism generating Alzheimer-like cytoskeletal inclusions initiated by mitochondrial dysfunction
The aim of this project is to understand the mechanism initiated by mitochondrial dysfunction leading to the accumulation of cytoskeletal inclusions containing hyperphosphorylated tau in neurons.
Dystrophic neuritic morphology and progressive loss of synapses are prominent events in Alzheimer’s disease (AD) involved in the progressive loss of memory in affected individuals. Both of these features implicate modification of the underlying microtubule and actin cytoskeletal networks. This laboratory is interested in how the AD-associated proteins Aβ and microtubule-associated protein tau participate in cytoskeletal dysfunction.
The available project uses primary neuronal cell culture, fluorescence microscopy and live-cell imaging to visualize and quantify the formation of neuritic inclusions and determine protein-protein interactions involved. Other tools used include molecular biology, live-cell motility assays, immunoprecipitation and Western blotting.
This lab is offering a PhD postgraduate scholarship to suitably qualified candidates (honours degree in cell biology, biochemistry, medical sciences or related field) valued at $19,616 pa to $25,000 pa (tax exempt) depending upon the applicant’s academic performance and standing.
Research in Dr. Goldsbury’s laboratory is funded by grants from the Sir Zelman Cowen Universities fund, the Mason Foundation and the Rebecca Cooper Foundation.
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The opportunity ID for this research opportunity is: 801