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Crowston Jonathan Guy

Professor

Senior Consultant Glaucoma,  Singapore National Eye Centre

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Dr Crowston is a Professor of Ophthalmology in the Neuroscience and Behavioural Disorders programme at Duke-NUS Medical School, and a glaucoma consultant at the Singapore National Eye Centre. His research focuses on understanding why ageing predisposes individuals to optic nerve damage in glaucoma, and developing new therapeutic approaches to boost neuronal repair.

He obtained his medical degree at the Royal Free Hospital SOM, London, and a PhD at University College London. Following ophthalmology training at Moorfields Eye Hospital, he completed glaucoma fellowships at Westmead Hospital in Sydney and the University of California, San Diego. He was subsequently appointed as a faculty member in the University of California, San Diego, and served as Director of the Hamilton Glaucoma Center Basic Research Laboratories. He moved to Melbourne in July 2006 and established the Glaucoma Research Laboratory at the Centre for Eye Research Australia (CERA). He was subsequently appointed as Head of Ophthalmology at the University of Melbourne and Director of CERA.

The goal of our research is to understand why advancing age predisposes to loss of retinal ganglion cells and from this determine new therapeutic approaches for protecting the optic nerve in glaucoma and other optic neuropathies.

We have discovered that retinal ganglion cells in mice enter a “comatose” non-functional state after injury but retain the capacity for functional recovery. Age is a major determinant of how well retinal ganglion cells recover following an acute intraocular pressure challenge. Importantly, this negative effect of aging is modifiable. Diet restriction and exercise profoundly improving the rate of functional recovery and synapse reformation. A specific focus is the role of bioenergetic compromise on retinal ganglion cell vulnerability.  Together with Ian Trounce in Melbourne we have demonstrated impaired mitochondrial activity in glaucoma patients, specifically in complex-I of the electron transport chain (OXPHOS). We are now aiming to uncover the key pathways involved in driving neurorecovery.

Another key area of our research is to develop diagnostic tests that inform on the state of RGC health. We believe these are needed to facilitate translation of candidate neuroprotective treatments into clinical trial. Functional recovery is increasingly recognised in response to treatment in human glaucoma. We have recently completed a clinical trial demonstrating visual recovery in human glaucoma in response to nicotinamide, a larger clinical study is in train.

  1. Hadoux X, Hui F, Lim JKH, Masters CL, Pebay A, Chevalier S, Ha J, Loi S, Fowler CJ, Rowe C, Villemagne VL, Taylor EN, Fluke C, Soucy JP, Lesage F, et al. Non-invasive in vivo hyperspectral imaging of the retina for potential biomarker use in Alzheimer's disease. Nat Commun. 2019;10(1):4227.
  2. Fry LE, Fahy E, Chrysostomou V, Hui F, Tang J, van Wijngaarden P, Petrou S, Crowston JG. The coma in glaucoma: Retinal ganglion cell dysfunction and recovery. Prog Retin Eye Res. 2018;65:77-92.
  3. Crowston J, Trounce I. Relief for retinal neurons under pressure. Science. 2017;355(6326):688-9.
  4. Chrysostomou V, Galic S, van Wijngaarden P, Trounce IA, Steinberg GR, Crowston JG. Exercise reverses age-related vulnerability of the retina to injury by preventing complement-mediated synapse elimination via a BDNF-dependent pathway. Aging Cell. 2016;15(6):1082-91.
  5. Chrysostomou V, Kezic JM, Trounce IA, Crowston JG. Forced exercise protects the aged optic nerve against intraocular pressure injury. Neurobiol Aging. 2014;35(7):1722-5.
  6. Crowston JG, Kong YX, Trounce IA, Dang TM, Fahy ET, Bui BV, Morrison JC, Chrysostomou V. An acute intraocular pressure challenge to assess retinal ganglion cell injury and recovery in the mouse. Exp Eye Res. 2015;141:3-8.
  7. O'Neill EC, Gurria LU, Pandav SS, Kong YX, Brennan JF, Xie J, Coote MA, Crowston JG. Glaucomatous optic neuropathy evaluation project: factors associated with underestimation of glaucoma likelihood. JAMA Ophthalmol. 2014;132(5):560-6.
  8. Chrysostomou V, Crowston JG. The photopic negative response of the mouse electroretinogram: reduction by acute elevation of intraocular pressure. Invest Ophthalmol Vis Sci. 2013;54(7):4691-7.
  9. Kong YX, van Bergen N, Bui BV, Chrysostomou V, Vingrys AJ, Trounce IA, Crowston JG. Impact of aging and diet restriction on retinal function during and after acute intraocular pressure injury. Neurobiol Aging. 2012;33(6):1126 e15-25.
  10. Kong YX, Van Bergen N, Trounce IA, Bui BV, Chrysostomou V, Waugh H, Vingrys A, Crowston JG. Increase in mitochondrial DNA mutations impairs retinal function and renders the retina vulnerable to injury. Aging Cell. 2011;10(4):572-83.
  11. Van Bergen NJ, Wood JP, Chidlow G, Trounce IA, Casson RJ, Ju WK, Weinreb RN, Crowston JG. Recharacterization of the RGC-5 retinal ganglion cell line. Invest Ophthalmol Vis Sci. 2009;50(9):4267-72.
  12. Kong YX, Crowston JG, Vingrys AJ, Trounce IA, Bui VB. Functional changes in the retina during and after acute intraocular pressure elevation in mice. Invest Ophthalmol Vis Sci. 2009;50(12):5732-40.
  13. Crowston JG, Akbar AN, Constable PH, Occleston NL, Daniels JT, Khaw PT. Antimetabolite-induced apoptosis in Tenon's capsule fibroblasts. Invest Ophthalmol Vis Sci. 1998;39(2):449-54.