Why faulty mitochondria could hold the key to age-related eye diseasesJune 21, 2017
Associate Professor Ian Trounce is a Principal Research Fellow in glaucoma research at the Centre for Eye Research Australia (CERA). He specialises in the study of mitochondria dysfunction
in the cell and how this fault relates to age-related neurodegenerative diseases of the optic nerve. His research scope also extends to other neurodegenerative disorders where mitochondrial dysfunction is strongly implicated, especially Parkinson’s disease.
A/Prof Trounce spoke recently to CERA colleague and Deputy Director, Professor Robyn Guymer, in the first of a video series focusing on researchers talking to each other about their research challenges. The full interview can be found by clicking here.
“Mitochondria are very much involved in the proper functioning of the eye, and we are pursuing why certain age-related eye diseases occur and where there is a mitochondrial component,” says A/Prof Trounce.
The overall question A/Prof Trounce is looking at is about energy in the cells and why a lack of energy in the mitochondria causes the optic nerve to degenerate with ageing. He is also looking at mitochondrial genetics, a topic deeply woven into A/Prof Trounce and his team’s research.
“Mitochondria have their very own piece of DNA, it comes only from the mother, and when that mitochondria DNA has certain errors or mutations it causes havoc. The optic nerve is affected as is the macular and that has given us a clue as to whether glaucoma, in particular, has mitochondrial genetic changes,” he says.
” Are you saying there is some problem with the energy supply to the optic nerve, is that your underlying hypothesis?” asks Professor Guymer.
“The optic nerve seems to be at the limit of biological organisation, so a bit less energy is a problem but it doesn’t seem to be a problem for the rest of the cells in the human body. If we could boost the energy levels in the cells just a little bit, it might make all the difference for someone with glaucoma and help them keep their vision,” A/Prof Trounce says.
“We have found there is a measurable defect in the energy supply levels in the mitochondria cells of patients with glaucoma and are exploring a pioneering path.
“A recent paper published in Science, which Jonathan Crowston and I commented on, was right up our alley because it identifies that a dietary supplement, vitamin B3 could have a protective effect on glaucoma in mice. We are likely to see a boost in this research area with more papers coming out in the coming years,” he says.
A/Prof Trounce says that one of the main benefits of working with CERA is the wonderful clinicians to collaborate with as there is huge buy in from patients because of CERA.
“Working with patients means we can be absolutely sure of the phenotype of the patients, which is often taken for granted,” A/Prof Trounce adds.
A/Prof Trounce then talks about the next steps for his CERA research team.
“We are working on mitochondrial diseases that affect the eye, such as Leber hereditary optic neuropathy (LHON), a disease that looks a lot like glaucoma in how the optic nerve is affected.
“One of the interesting questions is why men are more than five times more likely to contract the disease, and we are also looking at potential hormonal affects and how they impact the cell model,” A/Prof Trounce says.