Thanks to the work of NEI scientists and grantees, we’re constantly learning new information about the causes and treatment of vision disorders. Get the latest updates about their work — along with other news about NEI.
In a pair of papers on retinal structure, Duke University neurobiologists have shown that the rigors of natural selection and evolution have shaped the retinas in our eyes just as this theory of optimization would predict.
Researchers have developed a new gene therapy that could eventually provide an alternative treatment for Fuchs’ endothelial corneal dystrophy, a genetic eye disease affecting roughly one in 2,000 people globally.
Two translational studies at the Vanderbilt Eye Institute are targeting photoreceptors and retinal ganglion cells (RGCs) to restore vision through regeneration of the retina. The research is funded by the NEI Audacious Goals Initiative.
A form of gene therapy protects optic nerve cells and preserves vision in mouse models of glaucoma, according to research supported by NIH’s National Eye Institute. The findings suggest a way forward for developing neuroprotective therapies for glaucoma.
As regenerative therapies for blinding diseases move closer to clinical trials, the NEI's functional imaging consortium is pioneering noninvasive technologies to monitor the function of the retina’s neurons and their connections to the brain.
Researchers at the University of Wisconsin have developed a micro-molded scaffolding photoreceptor “patch” designed to be implanted under a damaged or diseased retina.
NEI-funded research at the University of Rochester has led to the development of a 3D lab model that mimics the part of the human retina affected in age-related macular degeneration.
The National Eye Institute (NEI) Data Commons now enables researchers to access data from patients with macular degeneration who participated in the Age-related Eye Disease Study 2 (AREDS2).
In a massive screen of 400 mouse genes, Yale School of Medicine researchers have identified 40 genes actively involved in suppression of axon regeneration in central nervous system cells.
