Dr. Grossman’s Blog

Researchers at Washington University School of Medicine in St. Louis have identified an intricate process that allows the human eye to adapt to darkness very quickly, as well as the process by which the eye can function in bright light.

This research will help scientists better understand human diseases that affect the retina, including age-related macular degeneration (AMD).

The retina’s main light-sensing cells are called rods and cones.   Cone cells allow us to see colors and can adapt to rapid changes in light intensity.   Cones use light-sensing molecules that bind together to make up visual pigments which are destroyed when they absorb light.  They must be rebuilt, or recycled, for the cone cells to continue sensing light. After exposure to light, key components of pigments called chromophores can leave the cells and travel to the nearby pigment epithelium near the retina. There the chromophore is restored and returned to the photoreceptor cells.

Researchers removed the pigment epithelium layer in salamander retinas, so that pigment molecules could not be recycled that way.  When they exposed retinal cells both to bright light and to darkness they found that the rods no longer worked, but the cones continued to function properly, even without the eye’s pigment epithelium.

Scientists treated mouse retinas with a chemical that destroyed Müller cells, which support and interact with rods and cones.  The retinas were then exposed to bright light, followed by darkness.   

When the function of Müller cells was blocked the retinal visual pathway could not function because cones ran out of photopigment and could not adapt to dark. When the Müller cells function properly, cones in the mouse, primate and human retinas are able to function in bright light and adapt to darkness, independently of the pigment epithelium.

Study authors believe that in the future it may be possible to manipulate this pathway in the retina to improve vision when the other pathway, involving pigment epithelium, has been interrupted by injury or disease, such as age-related macular degeneration.

SOURCE:  Wang, et al, “An alternative pathway mediates the mouse and human cone visual cycle”, Current Biology vol. 19 (19), Oct. 13, 2009.
“Researchers discover mechanism that helps humans see in bright and low light”, http://mednews.wustl.edu/news/page/normal/14856.html

Researchers from the University of Washington and the University of Florida have used gene therapy to cure two monkeys of color blindness. 

An article published online in the journal Nature discusses the potential for this type of gene therapy to treat adult vision disorders involving cone cells, including color blindness and other retinal diseases.

Color blindness is an inherited disorder caused by a single defective or absent gene.  Jay Neitz, a professor of ophthalmology at the University of Washington (U.W.) School of Medicine and senior study author and his wife Maureen Neitz, also in the U.W. ophthalmology department, have identified this particular gene and developed a working virus vector to carry a functional copy of it.

Researchers injected the gene-carrying virus into the monkeys’ eyes. In about 20 weeks the monkeys attained full color vision and have shown no harmful side effects.

Color-blindness is a common genetic disorder, affecting more than 3.5 people in the United States, including about 8% of Caucasian men, leaving them unable to distinguish between red and green hues.

The research team hopes to be able to translate the findings into clinical trials for humans. The team used human genetic material in the monkeys in the interest of expediting future research.

SOURCE:  Colour blindness corrected by gene therapy, Nature doi:10.1038/news.2009.921