Discovering what triggers the death of retinal cells, or photoreceptors, may hold the key to stopping causes by a wide range of eye diseases which lead to blindness. While several blinding disorders are known to cause the breakdown of photoreceptors, scientists are now seeking to identify mechanisms in photoreceptors that could be targeted to prolong their survival.
Using preserved animal and human retinal tissue, the study looked at different diseases with a range of genetic mutations that caused photoreceptor death, such as age-related macular degeneration and retinal pigmentosa.
While photoreceptors die from a variety of causes, this research found that all of the diseases had one common element—activation of a family of molecules called CREB1/ATF1. It was unclear, however, whether CREB1/ATF1 contributed to photoreceptor loss, or was an attempt by photoreceptors to delay their death.
To differentiate between these two possibilities, this study examined CREB1/ATF1 in retinas treated with a drug known to preserve photoreceptors. Protected photoreceptors expressed much higher amounts than unprotected retinas, suggesting that CREB1/ATF1 was part of the protective mechanism.
Not only did it show that the drug activated the novel CREB1/ATF1 photoreceptor pathway, but it was 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.
By finding a common way in which photoreceptors react to stress, it may soon be possible to develop new therapies to preserve vision.