A research conducted in Yale School of Medicine claims that determining what activates the death of retinal cells known as photoreceptors, could be crucial in halting blinding disorders caused by an extensive variety of eye diseases.
Numerous blinding disorders are supposedly known be the reason for breakdown of photoreceptors.
Caroline Zeiss, associate professor of comparative medicine and ophthalmology at Yale School of Medicine, and her colleagues sought to detect a mechanism in photoreceptors that could be aimed to extend their survival. By means of preserved animal and human retinal tissue, they examined diverse diseases with a variety of genetic mutations that apparently caused photoreceptor death like age-related macular degeneration and retinal pigmentosa.
Zeiss and her team examined in the diseases that photoreceptors died due to numerous causes, but the team discovered that apparently all of the diseases had one common factor i.e. activation of a family of molecules known as CREB1/ATF1. It was uncertain, nevertheless, whether CREB1/ATF1 added to photoreceptor loss, or was an effort by photoreceptors to holdup their death. To distinguish between these two possibilities, the team apparently studied CREB1/ATF1 in retinas treated with a drug supposedly known to conserve photoreceptors. Sheltered photoreceptors are believed to have expressed higher quantity as compared to defenseless retinas, thereby signifying that CREB1/ATF1 was supposedly a part of the defensive method.
Zeiss commented, “Not only did we find that the drug activated the novel CREB1/ATF1 photoreceptor pathway, but we found that this activation was caused by stress. This suggests that CREB/ATF1 may be an innate protective response that could be used to achieve broad spectrum preservation of the retina.”
Zeiss added, “This is the first time that any protective signal within photoreceptors has been identified across such a broad range of eye diseases. By finding a common way in which photoreceptors react to stress, it may be possible to develop new therapies to preserve vision.”
Zeiss mentioned that the subsequent step in the research is to strive to recognize drug targets that may perhaps trigger the CREB1/ATF1 pathway.
The finding was published in the Journal Investigative Ophthalmology and Visual Science.