Do We Need Optic Nerve Head Astrocytes to Become Reactive in Glaucoma?

Daniel Sun, PhD Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary (Harvard)


We still don’t know how people lose their vision in glaucoma. To date, we have a strong idea of where in the eye the damage begins, but the biological processes happening at this location, and the cells that are involved, remain unclear. This is important to find out if we want to be able to better target therapeutic interventions. My research focuses on better understanding the role that a type of supporting cell, called astrocytes, plays in the biological process of glaucoma, primarily whether they help to slow down the vision loss in glaucoma or make it worse.

Project Details

My research focuses on understanding the role that a type of supporting cell called astrocytes play in the biological processes of glaucoma, including whether they help to slow down the vision loss or make it worse. We will use transgenic mice, with specific gene knock-outs, to manipulate the function of these astrocytes and then test the effect this change of function has on cell survival and visual function following experimental glaucoma and an optic nerve crush injury. The results will help to determine whether astrocyte function in glaucoma should be suppressed or promoted and what biological pathways are involved, and having this knowledge could provide new ways of protecting the optic nerve.

There is currently no cure for glaucoma or neuroprotective treatment that directly targets the pathogenic mechanisms in the retina or optic nerve. To improve patient outcome, more treatment options are required. An important step towards alternative treatments is to better understand the pathogenic mechanisms underlying glaucoma. This involves going beyond simply studying the retinal ganglion cells themselves (ie, the cells that undergo damage and death from glaucoma), to understanding the potential role of supporting cells that support the ganglion cells, including astrocytes.