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Full-Text Articles in Ophthalmology

Melanopsin-Expressing Retinal Ganglion Cells In Control Vs. Glaucomatous Retinas, Edward Hamad Jan 2020

Melanopsin-Expressing Retinal Ganglion Cells In Control Vs. Glaucomatous Retinas, Edward Hamad

Williams Honors College, Honors Research Projects

Glaucoma is a common cause of vision loss worldwide and has a large scope of symptoms, ranging from pupillary reflex defects to sleep disorders. These issues can be explained partially by a recently found subtype of retinal ganglion cells that express melanopsin, denoted melanopsin-expressing retinal ganglion cells or mRGCs for short. These cells function primarily as photoreceptors in the non-image forming pathway, but can receive input from rods and cones. Since mRGCs play a role in the pupillary reflex and regulation of the sleep-wake cycle, I investigated if glaucoma leads to the degeneration of these cells in a mouse model …


A Clinico-Pathological Study Of The Structural And Functional Changes In The Retina And Optic Nerve Following Diabetic Retinopathy Treatments, Richard Filek Sep 2017

A Clinico-Pathological Study Of The Structural And Functional Changes In The Retina And Optic Nerve Following Diabetic Retinopathy Treatments, Richard Filek

Electronic Thesis and Dissertation Repository

Diabetic retinopathy (DR) is the result of microvascular changes in the retina due to hyperglycemia which alter the blood-retinal barrier (BRB). The increased permeability of BRB results in the accumulation of extracellular fluid, the development of diabetic macular edema (DME) and capillary occlusion. Capillary occlusion results in retinal ischemia which increases vascular endothelial growth factor (VEGF) levels, increases vascular permeability and results in neovascularization in proliferative diabetic retinopathy (PDR) patients. The treatments clinically used for DR are panretinal photocoagulation (PRP) for PDR and injectable vascular endothelial growth factor inhibitors (anti-VEGFs) for DME.

The safety of PRP and anti-VEGF therapy on …