Madrid. Using laboratory-grown worms, as well as human and mouse eye tissues, researchers at the University of Maryland School of Medicine (Omson) in the United States have identified a potential new mechanism for age-related macular degeneration, the leading cause of blindness among the elderly.
The discovery offers the potential to identify new molecular targets for treating the disease, according to its authors in the journal Measures From the US National Academy of Sciences.
The Omson researchers confirm that the results indicate a new and different reason for the previous approach indicating a failure in the immune system, which indicates that the structural organization of eye cells that detect light can be affected by disease.
According to the National Eye Institute, more than 14 percent of Americans over the age of 80 have age-related macular degeneration, which causes gradual loss of vision without known treatment. There is a treatment for the “wet” version of the disease that affects only 10 percent of cases, meaning most of them have no options.
“To find a cure for a disease, you have to understand its causes well, and we have identified new potential factors that were not known,” said Bruce Vogel, a physician, associate professor of physiology and a scientist at the Center for Biomedical Engineering and Technology. Omson.
Several years ago, researchers identified genetic mutations in the complement factor H protein as an element that contributes to a large number of macular degeneration cases, which distinguishes the body’s cells as its own and protects them from immune system attack, the task is to eliminate invading pathogens and cells that do not match.
Therefore, due to this protein’s role in this process, it was thought that macular degeneration might be due to the immune system attacking body cells that were not properly identified as “special”.
According to Vogel, because the identification of effective new treatments for the disease was slow, he wanted to see if his team could find new insights from studying the components of the disease in his laboratory model of roundworm. C. elegans.
Vogel’s team discovered a worm version of the complementary factor H protein found in sensory neurons that helps worms discover chemicals, food, touch and temperature.
The protein appeared specifically in the central region of the delicate antennas of sensory neurons, known as cilia (which perform the function of sensing the environment), next to another well-known airway protein called inversin. However, in worms that were bred to lack complementary factor H, they found that the reflector propagates through the antennae rather than staying at the center of the antennae.
Then the researchers confirmed their findings in light-detecting cells in human retinal tissues. Complement factor H and inversin had the same side-by-side position on the antenna of cells taken from intact samples.
However, in subjects with complementary H factor mutations (i.e., subjects genetically predisposed to macular degeneration), they found that invertersin was ubiquitous, and was not limited by the antenna-ordered band pattern.
“Our findings indicate that complementary factor H plays a role in maintaining photoreceptor cilia regulation and that this process may be flawed in age-related macular degeneration. We plan to continue this work to determine how this structural change affects vision, if we can reverse it and recover The function of these receptors, “added Vogel.
“Age-related blindness is an untreated condition that will become more prevalent as the population ages,” recalls Albert Rees, Executive Vice President for Medical Affairs at the University of Maryland Baltimore and Distinguished Professor Akiko Powers of the University of Maryland School. Of medicine.