
New research findings suggest that aging immune cells increase the risk for age-related macular degeneration (AMD). More specifically, aging macrophages can contribute to the inflammation and abnormal blood vessel growth in AMD. The recently published study in the journal JCI Insight comes from a team of researchers from the Washington University School of Medicine in St. Louis.
“By understanding what happens with the immune cells in the eye, it may be possible to develop therapies to help patients who can’t be helped with existing drugs,” says senior researcher Rajendra S. Apte, MD, PhD, a Distinguished Professor of Ophthalmology and Visual Sciences.
Apte and his team found that older macrophages carry larger amounts of microRNAs, which help regulate gene expression. In particular, microRNA-150 was found to be significantly abundant in macrophages in the eyes of older mice. In the team’s mouse model of macular degeneration, microRNA-150 seemed to be guiding older macrophages in promoting inflammation and abnormal blood vessel formation.
When the team compared blood samples from patients with and without AMD, those with AMD also had significantly higher levels of microRNA-150 in their macrophages.
“We think microRNA-150 may be a potential therapeutic target, or at least a biomarker, for aggressive disease and risk of vision loss,” said Jonathan B. Lin, first author of the study and an MD/PhD student at the School of Medicine. “Macular degeneration therapies seem to be treating disease symptoms, rather than its cause. We focused on the role of macrophages in regulating inflammation and the growth of abnormal blood vessels to see whether it may be possible one day to help people who don’t get much benefit from existing treatments and design therapies that may prevent progression to advanced forms of the disease.”
“It’s possible to envision immune-based therapies that would tweak the level of microRNAs so that these macrophage cells no longer contribute to disease,” said Apte. “Such therapies are a long way off, and we need to do a lot more research, but if we could make these older cells more like the younger ones, we might be able to prevent a great deal of vision loss.”
See the full press release here.
Source: Washington University School of Medicine