Dr Richard Gordon

Honorary Associate Professor

UQ Centre for Clinical Research
Faculty of Medicine

Overview

Dr. Richard Gordon leads a multi-disciplinary, industry-partnered research program in Translational Neuroscience which integrates immunology, drug development, pharmacology, metabolomics and microbial metagenomics. His group aims to understand and therapeutically target key pathological mechanisms which drive the onset and progression of neurodegenerative disorders such as Parkinson’s disease (PD) and Amyotrophic Lateral Sclerosis (ALS). Their work combines target validation studies in human patients with mechanistic insights from disease models to develop and test novel therapeutic strategies that can be translated towards clinical trials.

Key research themes within this program include:

  • Understanding how chronic immune and inflammasome activation contribute to neurodegeneration in the CNS
  • The role of gut dysbiosis and gastrointestinal dysfunction in Parkinson’s disease pathophysiology
  • Therapeutic targeting of the gut-brain axis for neuroprotection
  • Drug discovery, development and repositioning for novel therapeutic targets
  • Discovery and validation of clinical biomarkers for PD and ALS
  • Clinical trials for disease-modifying therapeutic strategies

Research Interests

  • Understanding and targeting the gut-brain axis in neurodegeneration
  • Targeting immune and inflammatory mechanisms for neuroprotection
  • Novel therapeutic approaches for regeneration of the central nervous system
  • Clinical bio-markers for early detection of Parkinson's disease
  • In silico approaches for therapeutic development
  • Drug repositioning to accelerate new treatments for progressive neurodegenerative disorders

Research Impacts

Dr. Gordon’s research has contributed to ground-breaking advances in the field of neuroinflammation and Parkinson’s disease, including discovery of a novel signalling paradigm for prokineticin signalling during neurodegeneration, and inflammasome activation as a driver of synuclein pathology and disease progression in PD. He established the Queensland Drug Repurposing Initiative (QDRI) which aims to accelerate new treatments for neurological diseases through drug repositioning. He is the Research Lead for the COMBO-PD clinical trial at UQ which is evaluating the therapeutic potential of restoring beneficial gut microbiota which are depleted in people with PD.

Dr. Gordon is a Board-certified toxicologist with the American Board of Toxicology (DABT) and has served as a member of the Gene Technology Technical Advisory Committee for the Australian Federal Government. He is also a Science Ambassador for the World Parkinson Coalition (WPC) for Australia and the Asia Pacific Region.

Qualifications

  • Board Certified Toxicologist (DABT), American Board of Toxicology
  • Bachelor of Technology, Anna University
  • Doctor of Philosophy, Iowa State University

Publications

View all Publications

Available Projects

  • Gastrointestinal pathology and alterations in the gut microbiota are often early pathogenic changes seen in Parkinson's disease (PD) and other neurological disorders. Clinical studies suggest that gastrointestinal deficits in people with PD, can often precede cardinal motor symptoms, based on which clinical diagnosis is confirmed. Emerging evidence suggests that specific alternations in the gut microbiota and gastrointestinal deficits are associated with neuronal dysfunction, chronic immune activation and progressive neurodegeneration seen in PD. Our translational research program on the gut-brain axis combines innovative preclinical mechanistic studies in model systems, with powerful big-data analytics on our clinical cohorts to understand the role of gut dysbiosis and gastrointestinal dysfunction in PD, with a focus on therapeutically tractable mechanisms that are involved. We use these insights to develop and test novel and clinically relevant neuroprotective strategies by which to slow, stop or even reverse neurodegeneration in PD.

View all Available Projects

Publications

Featured Publications

Book Chapter

  • Albornoz, Eduardo A., Woodruff, Trent M. and Gordon, Richard (2018). Inflammasomes in CNS diseases. Inflammasomes: clinical and therapeutic implications. (pp. 41-60) edited by Mario D. Cordero and Elisabet Alcocer-Gómez. Cham, Switzerland: Springer International. doi: 10.1007/978-3-319-89390-7_3

  • Gordon, Richard and Woodruff, Trent M. (2017). Neuroinflammation as a therapeutic target in neurodegenerative diseases. Disease-modifying targets in neurodegenerative disorders: paving the way for disease-modifying therapies. (pp. 49-80) edited by Veerle Baekelandt and Evy Lobbestael. London, United Kingdom: Academic Press. doi: 10.1016/B978-0-12-805120-7.00003-8

  • Gordon, Richard and Woodruff, Trent M. (2017). Neuroinflammation as a therapeutic target in neurodegenerative diseases. Disease-modifying targets in neurodegenerative disorders. (pp. 43-64) edited by Veerle Baekelandt and Evy Lobbestael. Boston, MA, United States: Academic Press (Elsevier Press).

Journal Article

Conference Publication

  • Jayabalan, Nanthini, Roper, Katherine Kerry, Woodhouse, Helen M., Adam, Robert J., O'Sullivan, John D. and Gordon, Richard (2022). A Novel Role for Glucocerebrosidase 1 (GBA1) in Parkinson's Disease. Experimental Biology Meeting 2022, Philadelphia, PA United States, 2-5 April 2022. Hoboken, NJ United States: John Wiley and Sons. doi: 10.1096/fasebj.2022.36.S1.R5391

  • Gordon, Richard, Albornoz, Eduardo, Kanthasamy, Anumantha and Woodruff, Trent (2018). C5aR1 is required for a-synuclein mediated NLRP3 inflammasome activation. 27th International Complement Workshop (ICW), Santa Fe, NM, United States, Sep 16-20, 2018. Kidlington, Oxford, United Kingdom: Pergamon Press. doi: 10.1016/j.molimm.2018.06.247

  • Magalhaes, Ricardo J. Soares, Giacomin, Paul, Sarnyay, Zoltan, Kraeuter, Ann, Urich, Tim, Bengtsson, Mia, Jin, Shuting, Albornoz, Eduardo A., Gordon, Richard and Woodruff, Trent (2017). Gut microbiome changes induced by experimental trichuris muris infection are associated with decreased cognitive function in mice. 65th Annual Meeting of the American-Society-of-Tropical-Medicine-and-Hygiene (ASTMH), Atlanta, GA, United States, 13-16 November 2016. Deerfield, United States: American Society of Tropical Medicine and Hygiene.

  • Deora, Vandana, Mantovani, Susanna, Yerbury, Justin, Clark, Richard, Atkin, Julie, Lee, John, Gordon, Richard and Woodruff, Trent M. (2017). Motor neuron disease proteins activate complement and generate C5a. 16th European Meeting on Complement in Human Disease (EMCHD), Copenhagen, Denmark, 8-12 September 2017. Kidlington, Oxford, United Kingdom: Pergamon Press. doi: 10.1016/j.molimm.2017.06.144

  • Li, Rui, Lee, John D., Levin, Samantha, Gordon, Richard and Woodruff, Trent M. (2016). A pathogenic role for the C5a receptor, C5aR2, in mouse models of Huntington's and Parkinson's disease. The XXVI International Complement Workshop (ICW), Kanazawa, Japan, 4-8 September 2016. Muenchen, Germany: Elsevier. doi: 10.1016/j.imbio.2016.06.186

  • Gordon, Richard, Albornoz, Eduardo A., Kumar, Vinod, Zhou, Kiane, Garin-Michaud, Ashoka, Mantavani, Susanna, Kanthasamy, Anumantha G. and Woodruff, Trent M. (2016). Complement C5a activates microglial NLRP3 inflammasomes and drives neurodegeneration in Parkinson's disease through C5aR1. The XXVI International Complement Workshop (ICW), Kanazawa, Japan, 4-8 September 2016. Muenchen, Germany: Elsevier. doi: 10.1016/j.imbio.2016.06.146

  • Li, R., Levin, S., Lee, J., Gordon, R. and Woodruff, T. (2016). The complement C5a receptor, C5aR2 contributes to motor deficits in mouse models of Huntington's and Parkinson's disease. International Congress of Immunology (ICI), Melbourne, Australia, 21-26 August 2016. Weinheim, Germany: Wiley - VCH. doi: 10.1002/eji.201670200

  • Albornoz, E., Deora, V., Robertson, B. A., Cooper, M. A., Schroder, K., Woodruff, T. M. and Gordon, R. (2015). Paraquat activates the NLRP3 Inflammasome in microglia via the NADPH oxidase pathway. International Congress of Immunology (ICI), Melbourne, Australia, Aug 21-26, 2016. Weinheim, Germany: Wiley-Blackwell.

  • Mantovani, S., Gordon, R., Ngo, S., Pfluger, C., O'Sullivan, J., Noakes, P., Henderson, R., McCombe, P. and Woodruff, T. (2015). Peripheral immune complement activation in neurodegenerative disease. 25th Biennial Meeting of the International-Society-for-Neurochemistry Jointly with the 13th Meeting of the Asian-Pacific-Society-for-Neurochemistry in Conjunction with the 35th Meeting of the Australasian-Neuroscience-Society, Cairns Australia, 23-27 August 2015. Chichester, West Sussex, United Kingdom: Wiley-Blackwell. doi: 10.1111/jnc.13188

  • Mantovani, S., Li, R., Gordon, R., Kumar, V., Taylor, S. and Woodruff, T. M. (2013). Behavioural and pathological phenotyping of the C57BL/6J BACHD transgenic mouse model of Huntington’s disease. World Congress on Huntington’s disease, Rio de Janeiro, Brazil, 15-18 September 2013. Amsterdam, Netherlands: I O S Press.

Grants (Administered at UQ)

PhD and MPhil 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.

  • Gastrointestinal pathology and alterations in the gut microbiota are often early pathogenic changes seen in Parkinson's disease (PD) and other neurological disorders. Clinical studies suggest that gastrointestinal deficits in people with PD, can often precede cardinal motor symptoms, based on which clinical diagnosis is confirmed. Emerging evidence suggests that specific alternations in the gut microbiota and gastrointestinal deficits are associated with neuronal dysfunction, chronic immune activation and progressive neurodegeneration seen in PD. Our translational research program on the gut-brain axis combines innovative preclinical mechanistic studies in model systems, with powerful big-data analytics on our clinical cohorts to understand the role of gut dysbiosis and gastrointestinal dysfunction in PD, with a focus on therapeutically tractable mechanisms that are involved. We use these insights to develop and test novel and clinically relevant neuroprotective strategies by which to slow, stop or even reverse neurodegeneration in PD.