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About
Associate Professor Ian Trounce
Head of Mitochondria and Neurodegeneration
Associate Professor Ian Trounce’s laboratory focuses on mitochondrial genetic and functional impairments and their contribution to optic nerve fragility in ageing, especially glaucoma but also neurodegenerative diseases.
Associate Professor Ian Trounce
Head of Mitochondria and Neurodegeneration
BSc, PhD
Associate Professor Ian Trounce is Principal Investigator and Head of Mitochondria and Neurodegeneration research at CERA.
Following his PhD studies at the University of Melbourne, he undertook postdoctoral training in the laboratory of Doug Wallace at Emory University before returning to Australia to establish his own laboratory.
His research focus is on mitochondria and how defects in oxidative phosphorylation contribute to age-related neurodegenerative diseases, including diseases of the optic nerve. His expertise encompasses biochemical, molecular and cell biology and genetic approaches.
CERA’s glaucoma research focuses on molecular pathogenesis and neuroprotection of the optic nerve in glaucoma. Associate Professor Trounce supervises a research team investigating the cellular processes related to ageing and mitochondrial dysfunction that affect the vulnerability of retinal ganglion cells to injury.
This work is intended to develop new therapeutic approaches for protecting the optic nerve in glaucoma. His research scope extends to other neurodegenerative diseases where mitochondrial dysfunction is strongly implicated, especially Parkinson’s disease.
Key research questions
- Does a ‘mismatching’ of mitochondrial DNA and nuclear gene variants contribute to age-related diseases such as glaucoma and Parkinson’s disease?
Current projects
Selected publications
My team
Key collaborators
Funding and support
Current projects
Nuclear-mitochondrial genetics in glaucoma and Parkinson’s disease
Investigating if nuclear gene variants can combine with mitochondrial DNA variants to increase disease risk.
Selected publications
Editorial: Mitochondrial dysfunction and genetic variations in neuro-ophthalmology diseases.
Vallabh NA, Trounce I. Front Ophthalmol (Lausanne). 2024 Oct 30;4:1483607. DOI: 10.3389/fopht.2024.1483607
Increased Diabetes Complications in a Mouse Model of Oxidative Stress Due to ‘Mismatched’ Mitochondrial DNA.
Januszewski AS, Blake R, Zhang M, Ma B, Anand S, Pinkert CA, Kelly DJ, Jenkins AJ, Trounce IA. Antioxidants (Basel). 2024 Feb 1;13(2):187. DOI: 10.3390/antiox13020187
OXPHOS bioenergetic compensation does not explain disease penetrance in Leber hereditary optic neuropathy.
Lopez Sanchez MIG, Van Bergen NJ, Kearns LS, Ziemann M, Liang H, Hewitt AW, Mackey DA, Trounce IA. Mitochondrion. 2020 Sep;54:113-121. DOI: 10.1016/j.mito.2020.07.003. Epub 2020 Jul 18.
My team
Key collaborators
- Isabel Lopez Sanchez, CERA
- Jonathan Crowston, Duke University Singapore
- Doug Wallace, University of Pennsylvania
- Dan Mishmar, Ben Gurion University Israel
- Justin StJohn, University of Adelaide
Funding and support
Thank you to the following organisations for their support:
- NHMRC
- Kathleen Rankin Bequest
- Michelmore Foundation
- DHB Foundation
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