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职业迁徙
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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.
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.
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Journal of glaucoma (2024)
Clinical & experimental ophthalmologyno. 4 (2023): 289-290
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Vicki Chrysostomou,Katharina C Bell,Sze Woei Ng, Samyuktha Suresh, Gayathri Karthik, Marion Millet, Yingying Chung,Jonathan G Crowston
Experimental eye research (2023): 109722-109722
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