Attributions

Protection of ONH astrocytes and structure in glaucoma

Peter Koulen, PhD University of Missouri at Kansas City

Summary

Degeneration or acute damage of the retina due to glaucoma related disease processes is a major cause of visual loss and blindness in the United States and worldwide. As glaucoma affects significant and increasing portions of the U.S. population including minorities affected by disparities in health care delivery, determining causes, mechanisms of action and subsequently potential treatment strategies will contribute to improving health care, health and performance requiring visual tasks. This study uses a novel mechanism underlying a self-defense mechanism of the retina to protect a critical structure of the retina, the optic nerve head, in order to develop new treatment strategies that have the potential to be complementary in nature to current strategies aimed at neuroprotection or aimed at lowering intraocular pressure.

Project Details

Degeneration or acute damage of the retina due to glaucoma related disease processes is a major cause of visual loss and blindness in the United States and worldwide. As glaucoma affects significant and increasing portions of the U.S. population including minorities affected by disparities in health care delivery, determining causes, mechanisms of action and subsequently potential treatment strategies will contribute to improving health care, health and performance requiring visual tasks. This study uses a novel mechanism underlying a self-defense mechanism of the retina to protect a critical structure of the retina, the optic nerve head, in order to develop new treatment strategies that have the potential to be complementary in nature to current strategies aimed at neuroprotection or aimed at lowering intraocular pressure.

Our approach is characterized by two novel aspects for glaucoma research and glaucoma therapy development:
  1. Identification and use of a novel drug target in mitochondria of optic nerve head astrocytes (ONHA)
  2. Targeting ONHA activation, dysfunction and degeneration along with a pathological re-structuring of the ONH extracellular matrix in a novel intervention approach that has the potential to be complementary in nature to current strategies aimed at neuroprotection or aimed at lowering intraocular pressure.