Mae'r cynnwys hwn ar gael yn Saesneg yn unig.
Glaucoma remains one of the major causes of vision loss. Current treatments are focused on the reduction of intraocular pressure, which is the main modifiable risk factor. However, a growing body of evidence suggests that other factors and in particular, the general health of the patient may be important in determining the degree of retinal damage at any given intraocular pressure. Recent work in patients with Alzheimer’s disease (which shares pathophysiological mechanisms with glaucoma) suggests that the general level of systemic inflammation can adversely affect neuronal health; patients with more inflammation are at greater risk of progressive dementia. Extrapolation of these phenomena to glaucoma raises the prospect that inflammatory mechanisms could influence the rate of glaucoma damage. In my PhD I will explore this possibility by examining the relationship between systemic levels of inflammation and the degree of glaucoma damage using a model of experimental glaucoma. We will focus on activation of the innate immune system on retinal neuronal health to see if therapeutic interventions to reduce this inflammation can be used to limit glaucoma damage.
Participation in practical demonstrations in the module: OP1206 Ocular Anatomy and Physiology
Honours and Awards
2016: Technological Educational Institute of Athens: Award for the highest degree grade of June 2016 class
2017-2020: PhD studentship from the School of Optometry and Vision Sciences, Cardiff University
Educational and Professional Qualifications
2017-Present: PhD, A tooth for an eye? The role of innate immune activation in glaucoma, Cardiff University
2016-2017: M.Sc., Investigative Ophthalmology and Vision Science (Distinction), The University of Manchester
2011-2016: B.Sc., Optics and Optometry (First-Class Honours), Technological Educational Institute of Athens
Dendritic loss is a marker of retinal ganglion cell degeneration, occurring before cell death, in early glaucoma models. In our lab, diolistic labelling of RGC structure (see figure 1 for a representative picture, kindly provided by Dr. James Tribble) followed by Sholl analysis has been successfully used to determine the amount of dendritic loss in experimental glaucoma. I will use that method, as well as biolistic transfection using synaptic markers to measure connectivity, to investigate the changes occurring in RGC dendrites in experimental glaucoma with coexisting systemic inflammation and after the administration of therapeutics that limit complement activation. I will also perform ERGs (photopic negative responses) to assess the functional impact of glaucoma and novel therapeutics.
Fight For Sight