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Associate Professor Shyuan Ngo

Principal Research Fellow

Australian Institute for Bioengineering and Nanotechnology
s.ngo@uq.edu.au
+61 7 344 31133

Overview

I completed my undergraduate and PhD training at UQ. After completing my PhD in 2009, I took up a postdoctoral position at UQCCR to introduce a translational edge to my research program. In 2012, I was awarded a Bill Gole Postdoctoral Research Fellowship from the Motor Neurone Disease Research Institute of Australia (MNDRIA) and returned to the School of Biomedical Sciences with this fellowship to continue my research program in motor neuron disease (MND). In 2015, I was awarded the Scott Sullivan MND Research Fellowship. In this position, I conduct research between the Australian Institute for Bioengineering and Nanotechnology and the Queensland Brain Institute at UQ, and the Royal Brisbane and Women's Hospital and the Wesley Hospital to address how changes in energy metabolism affects the course of MND, whilst working to develop therapies for MND.

The primary interest of my research group is to understand how metabolic homeostasis at the systemic and cellular level can impact upon neurodegenerative processes. My group's Metabolic Exploration in Neurodegenerative Disease (MEND) research program centres on Motor Neurone Disease (MND), a fatal neurological condition in which the average life expectancy is 27 months following diagnosis. In MND, the irreversible degeneration of neurones in the central nervous system leads to progressive paralysis and eventually, death. There is no effective treatment for MND, and hence no cure. We are using mouse models of MND, and human myosatellite cell-derived muscle fibres and human induced pluripotent stem cell (iPSC)-derived neurons to not only understand the mechanistic nature of MND, but to also conduct preclinical testing of potential therapeutic compounds. The combined use of mouse and human-derived models are integral to our goal of translating research findings into clinical trials for MND.

Research Interests

  • Metabolic Dysfunction in Motor Neuron Disease/Amyotrophic Lateral Sclerosis
  • Biomarkers in Motor Neuron Disease/Amyotrophic Lateral Sclerosis
  • Neuromuscular Junction Formation, Maintenance and Stability

Qualifications

  • Doctor of Philosophy, The University of Queensland

Publications

View all Publications

Grants

View all Grants

Supervision

  • Deciphering the spatio-temporal landscape of cell-autonomous and non-cell-autonomous drivers of motor neuron death in MND

    Doctor Philosophy

  • Targeting metabolic flexibility as a therapeutic approach for amyotrophic lateral sclerosis (METALS)

    Doctor Philosophy

  • Fine tuning metabolic flux: Modulating substrate oxidation as a therapeutic strategy in motor neuron disease (MND)

    Doctor Philosophy

View all Supervision

Available Projects

  • Metabolic dysfunction in Motor Neuron Disease/Amyotrophic Lateral Sclerosis

    Motor Neuron Disease/Amyotrophic Lateral Sclerosis (MND/ALS) is a neurodegenerative disease that is characterised by the degeneration of both upper and lower alpha motor neurons. The irreversible loss of neurons in the brain and spinal cord results in progressive skeletal muscle paralysis and death within 2-5 years of diagnosis. There is no known cure for the disease, and treatments are of limited benefit. In the absence of a cure for MND/ALS, there is a pressing need to lessen the severity of symptoms associated with, and to slow the progression of disease, whilst enhancing quality of life.

    While the fundamental mechanisms that underlie the development of MND/ALS remains unknown, recent studies suggest that defective regulation of energy homeostasis may exacerbate the degenerative process throughout the course of disease. In the last 7 years, our team has made novel observations of metabolic dysfunction and altered metabolic flexibility in mouse models of MND, and paradigm-shifting discoveries that for the first time, highlight the impact of increased energy use (hypermetabolism) in patients with MND on disease progression and prognosis. In this time, our team have also successfully generated induced pluripotent stem cell (iPSC)-derived motor neurons (including CRISPR-Cas9 TDP-43 iPSCs with isogenic controls), and to our knowledge the only directly reprogrammed motor neurons from MMD patients in Australia.

    All PhD projects fall under a broader research program that investigates how altered glucose and fatty acid metabolism contributes to the progression of MND/ALS. Projects span the clinical and basic research settings, and involve working with patients living with MND, or mouse and human-derived models of MND. Projects focus on identifying the mechanisms that cause metabolic dysfunction in MND, and identifying treatments to alleviate metabolic perturbations.

View all Available Projects

Publications

Book Chapter

  • Diet, disease severity, and energy expenditure in amyotrophic lateral sclerosis (ALS)

    Castles, Zoe, Buckett, Lauren, Jiang, Leanne, Steyn, Frederik J. and Ngo, Shyuan T. (2023). Diet, disease severity, and energy expenditure in amyotrophic lateral sclerosis (ALS). Diet and nutrition in neurological disorders. (pp. 123-140) edited by Colin R. Martin, Vinood B. Patel and Victor R. Preedy. Amsterdam, Netherlands: Elsevier. doi: 10.1016/b978-0-323-89834-8.00007-6

  • Biofluid biomarkers of amyotrophic lateral sclerosis

    Holdom, Cory J., Steyn, Frederik J., Henderson, Robert D., McCombe, Pamela A., Rogers, Mary-Louise and Ngo, Shyuan T. (2022). Biofluid biomarkers of amyotrophic lateral sclerosis. Neurodegenerative diseases biomarkers: towards translating research to clinical practice. (pp. 263-306) edited by Philip V. Peplow, Bridget Martinez and Thomas A. Gennarelli. New York, United States: Springer . doi: 10.1007/978-1-0716-1712-0_11

  • High Caloric diets for amyotrophic lateral sclerosis

    Ngo, Shyuan T., Steyn, Frederik J., McCombe, Pamela A. and Borges, Karin (2015). High Caloric diets for amyotrophic lateral sclerosis. Bioactive nutraceuticals and dietary supplements in neurological and brain disease: prevention and therapy. (pp. 355-361) edited by Ronald Ross Watson and Victor R. Preedy. London, United Kingdom: Academic Press. doi: 10.1016/B978-0-12-411462-3.00036-9

  • Neurophysiological recording of the compound muscle action potential for motor unit number estimation in mice

    Ngo, Shyuan T. and Bellingham, Mark C. (2013). Neurophysiological recording of the compound muscle action potential for motor unit number estimation in mice. Stimulation and inhibition of neurons. (pp. 225-235) edited by Pilowsky, Paul M., Farnham, Melissa M. J. and Fong, Angelina Y.. New York, NY United States: Humana Press. doi: 10.1007/978-1-62703-233-9_13

Journal Article

Conference Publication

Other Outputs

Grants (Administered at UQ)

PhD and MPhil Supervision

Current Supervision

Completed Supervision

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • Metabolic dysfunction in Motor Neuron Disease/Amyotrophic Lateral Sclerosis

    Motor Neuron Disease/Amyotrophic Lateral Sclerosis (MND/ALS) is a neurodegenerative disease that is characterised by the degeneration of both upper and lower alpha motor neurons. The irreversible loss of neurons in the brain and spinal cord results in progressive skeletal muscle paralysis and death within 2-5 years of diagnosis. There is no known cure for the disease, and treatments are of limited benefit. In the absence of a cure for MND/ALS, there is a pressing need to lessen the severity of symptoms associated with, and to slow the progression of disease, whilst enhancing quality of life.

    While the fundamental mechanisms that underlie the development of MND/ALS remains unknown, recent studies suggest that defective regulation of energy homeostasis may exacerbate the degenerative process throughout the course of disease. In the last 7 years, our team has made novel observations of metabolic dysfunction and altered metabolic flexibility in mouse models of MND, and paradigm-shifting discoveries that for the first time, highlight the impact of increased energy use (hypermetabolism) in patients with MND on disease progression and prognosis. In this time, our team have also successfully generated induced pluripotent stem cell (iPSC)-derived motor neurons (including CRISPR-Cas9 TDP-43 iPSCs with isogenic controls), and to our knowledge the only directly reprogrammed motor neurons from MMD patients in Australia.

    All PhD projects fall under a broader research program that investigates how altered glucose and fatty acid metabolism contributes to the progression of MND/ALS. Projects span the clinical and basic research settings, and involve working with patients living with MND, or mouse and human-derived models of MND. Projects focus on identifying the mechanisms that cause metabolic dysfunction in MND, and identifying treatments to alleviate metabolic perturbations.

This staff member is a UQ Expert for media in the following fields:

Motor Neuron Disease

They are happy to lend their expertise to your articles or broadcasts and share their research discoveries and insights with the community via media channels.

For additional assistance with story ideas, general advice and information or help with seeking further experts, please email the UQ Media Team or telephone (07) 3365 1120.

Links

ResearcherID: O-3908-2016

ORCID: 0000-0002-1388-2108

Scopus ID: 7003395267

Personal Profile: Link

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