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Neurodegenerative disorders


   Institute for Glycomics

  Dr Thomas Ve  Applications accepted all year round  Funded PhD Project (Students Worldwide)

About the Project

We are currently looking for a PhD candidate to work on the following projects:

Understanding enzymes linked to neurodegeneration and antiviral defence: An ARC funded Future Fellowship. The primary focus of this role is to contribute towards characterising a novel class of enzymes involved in protecting bacteria against viral infection and destruction of nerve fibres (axons) in humans. These enzymes use an essential helper molecule found in all living cells called nicotinamide adenine dinucleotide (NAD+) as fuel, which sets off a series of events in the cell that can result in its self-destruction. One member of this enzyme family, SARM1 is a key executioner of axon degeneration and an attractive therapeutic target for many neurodegenerative disorders. Many other members of this enzyme family play an important role in bacterial defence systems against viruses, but the mechanism of how they use NAD+ to provide resistance against viral infection has not yet been explored. Mechanistic understanding of bacterial antiviral defence systems has previously led to the development of revolutionary biotechnological tools such as restriction enzymes and the genome -editing technology CRISPR-Cas9. Understanding the mechanism of new defence systems such as the ones using NAD+ as fuel may provide a foundation for developing new exciting molecular tools. This project combines innovative chemical and structural biology approaches to characterise NAD+ consuming enzymes at the molecular level; define how the enzymes are regulated; and explore the diversity and targets of the nucleotide signals produced by the enzymes.

Structural Biology and Therapeutic Targeting of Neurodegeneration:  

A National Health and Medical Research Council (NHMCR)-funded Investigator Grant. The primary focus of this role is to contribute towards characterising the biology and translational potential of SARM1, a key executioner of axon degeneration, and a promising new therapeutic target for neurodegenerative disorders. Neurodegenerative disorders have been predicted by the World Health Organisation to overtake cancer and become the second-most prevalent cause of death in the next 20 years. When nerve fibres (axons) are damaged, whether by injury, disease or as a side effect of certain drugs, a program is triggered to make axons self-destruct. This destruction plays an important role in multiple neurodegenerative conditions, including peripheral neuropathy, Parkinson's disease, amyotrophic lateral sclerosis (ALS), traumatic brain injury and glaucoma. There are no current treatments that effectively target axonal breakdown, but the enzyme SARM1 has become an attractive therapeutic target. In order to exploit the full promise of targeting SARM1, detailed knowledge of the SARM1 structure and the molecular mechanisms upstream and downstream of SARM1 enzyme activity is required. This project combines innovative chemical and structural biology approaches to characterise SARM1 and to identify new strategies for design of targeted inhibitors of axon degeneration, which can be developed into therapeutic agents for neurodegenerative disease.

For project related enquiries please contact:

Dr Thomas Ve

Phone: (07) 5552 7012

Email: 

For administration enquiries please contact:

Institute for Glycomics

Phone: (07) 5552 8051

Email: 

All applications must be submitted as set out below:

Interested applicants should submit and expression of interest (EOI) to  containing:

  • Statement addressing your suitability for the project/scholarship
  • A brief CV
  • Academic Transcript
  • Name and contact details of two references. It is advisable that at least one of the referees has direct knowledge of your laboratory and other skills, for example previous Honours or Masters supervisor or employer.

Currently open for expressions of interest (EoIs)

The preferred applicant will then be invited to apply on-line.


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