Overview
Background
Dr Eduardo Albornoz is a neuroimmunologist whose research focuses on how innate immune mechanisms contribute to neurodegenerative disease. His work investigates how inflammasome and complement pathways are activated by environmental, infectious, and disease-related triggers in conditions such as Parkinson’s disease and motor neuron disease.
Dr Albornoz has expertise in neuroscience, immunology, pharmacology, translational drug development, and preclinical disease modelling. His research integrates human microglia, brain organoids, viral infection models, and animal models to understand how neuroinflammation contributes to neuronal injury and disease progression.
He completed his PhD at The University of Queensland, where he contributed to the development of next-generation NLRP3 inflammasome inhibitors and helped validate NLRP3 as a therapeutic target in Parkinson’s disease. This work supported translational drug development programs that progressed towards clinical testing.
His current research program focuses on environmental and infectious drivers of neurodegeneration, including pesticides, microplastics, PFAS, SARS-CoV-2, and other neurotropic viruses. A major focus of his work is understanding how multiple environmental, infectious, and proteopathic “hits” interact to amplify chronic neuroinflammation and accelerate neurodegenerative disease progression. His research aims to identify therapeutic strategies targeting innate immune pathways to slow or prevent neurodegeneration.
Availability
- Dr Eduardo Albornoz Balmaceda is:
- Available for supervision
- Media expert
Fields of research
Qualifications
- Masters (Research) of Biochemistry, Universidad Andrés Bello
- Doctor of Philosophy of Neurosciences, The University of Queensland
Research interests
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Neuroinflammation and Neurodegeneration
Research focused on how innate immune pathways drive neurodegenerative diseases including Parkinson’s disease and motor neuron disease. Investigating how chronic neuroinflammation contributes to neuronal injury, disease progression, and therapeutic response
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Inflammasome and Complement Biology
Investigating the role of inflammasome and complement pathways in chronic neuroinflammation and neurodegeneration. Research aims to identify how these innate immune systems interact to amplify neuronal injury and contribute to disease progression.
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Environmental Drivers of Neurodegeneration
Research examining how environmental exposures, including pesticides, microplastics, and PFAS, contribute to neuroinflammation and neurodegenerative disease. Focused on understanding how multiple environmental and disease-related “hits” interact to drive chronic inflammatory responses in the brain.
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Viral Neuroimmunology
Investigating how viral infections, including SARS-CoV-2 and neurotropic flaviviruses, activate inflammatory pathways associated with neurodegeneration. Research includes mechanisms linking viral infection, cellular senescence, and chronic neuroinflammation.
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Human Microglia and Brain Organoids
Development and application of advanced human-relevant experimental models, including patient-derived microglia and brain organoids, to study neuroinflammation, neurodegeneration, and therapeutic responses in translational neuroscience research.
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Translational Neuroimmunology and Drug Development
Research focused on translating neuroimmunology discoveries into therapeutic strategies targeting innate immune pathways. Includes development and preclinical evaluation of immunomodulatory therapies for neurodegenerative disease.
Research impacts
Dr Albornoz’s research investigates how environmental, infectious, and disease-related factors trigger harmful inflammatory responses in the brain that contribute to neurodegenerative disease progression.
His work helped validate the NLRP3 inflammasome as a therapeutic target in Parkinson’s disease and contributed to the development of next-generation inflammasome inhibitors through collaboration with Inflazome, later acquired by Roche. His research has also contributed to understanding how complement and inflammasome pathways interact to amplify chronic neuroinflammation and neuronal injury in neurodegenerative disease. Together, this work formed part of translational drug development programs progressing towards clinical testing and contributed to one of UQ’s most successful biomedical commercialisation outcomes.
His studies on SARS-CoV-2, neuroinflammation, and cellular senescence provided some of the first mechanistic evidence linking viral infection to activation of inflammatory pathways associated with neurodegeneration. This work received international attention through extensive media coverage, strong citation impact, and recognition as a highly cited and “hot” publication.
A major focus of Dr Albornoz’s research is understanding how multiple environmental, infectious, and disease-related “hits” interact to amplify chronic inflammation, neuronal injury, cellular dysfunction, and self-sustaining cycles of immune activation in the brain. This work aims to improve understanding of modifiable disease risk factors and identify opportunities for earlier therapeutic intervention, disease prevention, and development of new immunomodulatory therapies.
His research also contributes to development of advanced human-relevant experimental models, including patient-derived microglia and human brain organoids, supporting more predictive preclinical testing and translational neuroscience research.
Through collaborations with academic, biotechnology, and clinical research partners, his work supports the translation of neuroimmunology discoveries into therapeutic development and improved understanding of neurodegenerative disease mechanisms.
Works
Search Professor Eduardo Albornoz Balmaceda’s works on UQ eSpace
2017
Journal Article
The ketone body β-hydroxybutyrate does not inhibit synuclein mediated inflammasome activation in microglia
Deora, Vandana, Albornoz, Eduardo A., Zhu, Kevin, Woodruff, Trent M. and Gordon, Richard (2017). The ketone body β-hydroxybutyrate does not inhibit synuclein mediated inflammasome activation in microglia. Journal of Neuroimmune Pharmacology, 12 (4), 1-7. doi: 10.1007/s11481-017-9754-5
2017
Conference Publication
Gestational hypothyroxinemia increases the immune response of the progeny that suffers experimental autoimmune encephalomyelitis
Opazo, Maria Cecilia, Bugueño, Katherinne, Jara, Evelyn, Haensgen, Henny, Albornoz, Eduardo, Gomez, Felipe, Binzberger, Rebecca, Toledo, Paola, Blanco, Noelia, Simon, Felipe, Elorza, Alvaro, Kalergis, Alexis, Bueno, Susan and Riedel, Claudia (2017). Gestational hypothyroxinemia increases the immune response of the progeny that suffers experimental autoimmune encephalomyelitis. Immunology 2017™ Meeting, Washington, DC United States, 12-16 May 2017. Rockville, MD United States: American Association of Immunologists. doi: 10.4049/jimmunol.198.supp.207.8
2017
Conference Publication
Gut microbiome changes induced by experimental trichuris muris infection are associated with decreased cognitive function in mice
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.
2016
Conference Publication
Complement C5a activates microglial NLRP3 inflammasomes and drives neurodegeneration in Parkinson's disease through C5aR1
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
2015
Journal Article
Gestational hypothyroidism increases the severity of experimental autoimmune encephalomyelitis in adult offspring (vol 23, pg 1627, 2013)
Albornoz, E. A., Carreno, L. J., Cortes, C. M., Gonzalez, P. A., Cisternas, P. A., Cautivo, K. M., Catalan, T. P., Opazo, M. C., Eugenin, E. A., Berman, J. W., Bueno, S. M., Kalergis, A. M. and Riedel, C. A. (2015). Gestational hypothyroidism increases the severity of experimental autoimmune encephalomyelitis in adult offspring (vol 23, pg 1627, 2013). Thyroid, 25 (9), 1068-1068. doi: 10.1089/thy.2012.0401.cxn
2015
Journal Article
Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species
Arriagada, Alejandro A., Albornoz, Eduardo, Cecilia Opazo, Ma., Becerra, Alvaro, Vidal, Gonzalo, Fardella, Carlos, Michea, Luis, Carrasco, Nancy, Simon, Felipe, Elorza, Alvaro A., Bueno, Susan M., Kalergis, Alexis M. and Riedel, Claudia A. (2015). Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species. Endocrinology, 156 (4), 1540-1551. doi: 10.1210/en.2014-1371
2015
Conference Publication
Paraquat activates the NLRP3 Inflammasome in microglia via the NADPH oxidase pathway
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.
2013
Journal Article
Gestational hypothyroidism increases the severity of experimental autoimmune encephalomyelitis in adult offspring
Albornoz, Eduardo A., Carreno, Leandro J., Cortes, Claudia M., Gonzalez, Pablo A., Cisternas, Pablo A., Cautivo, Kelly M., Catalan, Tamara P., Cecilia Opazo, M., Eugenin, Eliseo A., Berman, Joan W., Bueno, Susan M., Kalergis, Alexis M. and Riedel, Claudia A. (2013). Gestational hypothyroidism increases the severity of experimental autoimmune encephalomyelitis in adult offspring. Thyroid, 23 (12), 1627-1637. doi: 10.1089/thy.2012.0401
Funding
Past funding
Supervision
Availability
- Dr Eduardo Albornoz Balmaceda is:
- Available for supervision
Looking for a supervisor? Read our advice on how to choose a supervisor.
Available projects
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Environmental Drivers of Neuroinflammation in Parkinson’s Disease
This project investigates how environmental exposures, including pesticides, microplastics, and PFAS, contribute to chronic neuroinflammation and neurodegeneration in Parkinson’s disease. The student will use advanced human-relevant models, including patient-derived microglia and brain organoids, to study how environmental and disease-related factors interact to activate innate immune pathways.
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Viral Infection and Neurodegeneration
This project examines how viral infections, including SARS-CoV-2 and neurotropic viruses, trigger inflammatory responses associated with neurodegenerative disease. Research will focus on mechanisms linking viral infection, cellular senescence, and chronic neuroinflammation using translational human and preclinical models.
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Inflammasome and Complement Pathways in Neurodegenerative Disease
This project investigates how innate immune pathways, including inflammasome and complement signalling, contribute to neuronal injury and disease progression in Parkinson’s disease and motor neuron disease. The project will involve molecular, cellular, and translational neuroscience approaches to identify potential therapeutic targets.
Supervision history
Current supervision
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Doctor Philosophy
Therapeutic blockade of neuroinflammation for the treatment of Huntington's disease
Associate Advisor
Other advisors: Dr John Lee, Professor Trent Woodruff
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Doctor Philosophy
Pathomechanisms in Alzheimer's disease
Associate Advisor
Other advisors: Dr Pranesh Padmanabhan
Media
Enquiries
Contact Dr Eduardo Albornoz Balmaceda directly for media enquiries about:
- C5aR
- Complement system
- Drug discovery
- Immunology
- Infectious disease and brain
- Inflammasomes
- Long COVID
- Microglia
- Neuroimmunology
- Neuroinflammation
- Neuroscience
- NLRP3
- Parkinson's disease
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