Overview
- University of Minnesota researchers report that genetic removal of Nlrp3 curtailed subretinal immune cell infiltration and basal laminar deposits in mouse models.
- Findings published in Cell Death & Disease show protection in age-related paradigms and in a R345W Efemp1 model that forms AMD-like deposits.
- Investigators identify the inflammasome pathway as a promising target for interventions intended to avert early retinal pathology.
- The team plans to test whether similar anti-inflammatory approaches could reverse early disease and to pursue translational candidates, with no human data yet.
- AMD is the leading cause of vision loss for Americans 65 and older and affects nearly 20 million people, and the work was supported by agencies including the National Eye Institute.