IRAK-M Upregulation as an Approach to Slow the Progression of Macular Degeneration
Researchers here report that the IRAK-M protein is protective of retinal cell health, but the amount of IRAK-M expressed in the retina declines with age. This may be due to the increased oxidative stress that is characteristic of aged tissues. Gene therapy to increase IRAK-M expression appears to slow the progression of damage and loss of function in the retina in mice, at least in the models tested. It remains to be seen as to whether this will hold up in the condition itself.
Progression of age-related macular degeneration (AMD) affects around 200-million people worldwide. Patients suffering from AMD often start with blurred vision or seeing a black dot in their central vision, which can ultimately expand to the point where there is no useful central vision. The exact cause of AMD is complex and thought to involve a combination of aging, genetics, environment, and lifestyle factors. Primarily affecting people over the age of 50, the risk of developing AMD significantly increases with age and makes tasks like reading and driving difficult.
Scientists believe that chronic inflammation, which is typical with aging, is associated with the reduction of a key immune regulatory protein called IRAK-M. This protein is crucial for protecting the retinal pigment epithelium (RPE), a layer of cells essential for maintaining a healthy retina. When RPE cells are damaged, it can result in serious eye conditions and vision loss.
In this study, researchers investigated the role of IRAK-M in AMD by examining genetic variations and their link to AMD risk. By studying IRAK-M levels in patient samples and mouse models of retinal degeneration, the team observed changes in retinal function in mice lacking the IRAK3 gene, which expresses the IRAK-M protein. They found that IRAK-M decreases with age, especially in the retinal pigment epithelium (RPE), and this decline is more pronounced in those with age-related macular degeneration (AMD).
The team then sought to explore whether increasing IRAK-M could protect retinal cells from degeneration in mouse models and whether it is a potential therapeutic target for macular degeneration. They show that increasing IRAK-M levels through RPE-specific gene delivery helps protect against the effects of aging and oxidative stress and reduces retinal degeneration. The researchers aim to help develop the therapies further through a new spin-out company called Cirrus Therapeutics.
Link: https://www.bristol.ac.uk/news/2024/june/amd-study.html
A major problem with convincing people/society to act on aging is that young people who have the brains don't care because it's too long into the future before they get old and (hopefully) therapies will be availabe before they get old so they don't want to work on it because others are going to do it so they play video games instead. The old ones has brains that are degenerating and tjeir overall health decrease so they have a lot to think about. In fact so much that they can't set aside time to work on it. This gridlock/limbo must be breaked.