Investigating the role of SIGIRR in geographic atrophy type of age-related macular degeneration
Research details
- Type of funding: PhD Studentship
- Grant Holder: Dr Mei Chen
- Institute: Queen's University Belfast (QUB)
- Region: Northern Ireland
- Start date: October 2018
- End Date: May 2024
- Priority: Causes
- Eye Category: AMD
Age related macular degeneration (AMD) is the leading cause of blindness in the older population of developed countries. Inflammation is an important factor that damages the macula in AMD. Controlled inflammation may slow down or halt AMD progression. Too much inflammation can cause damage to the surrounding tissues and too little is ineffective in protection.
One molecule that can turn off the inflammatory process is called SIGIRR. Researchers have found that eyes donated from dry AMD patients have less SIGIRR when compared with eyes from healthy donors. Mice without SIGIRR developed dry AMD-like disease in the eye. The results suggested that insufficient SIGIRR may be a key factor for uncontrolled inflammation in AMD. Therefore, enhancing SIGIRR expression could be a novel approach for immune therapy.
Researchers aim to understand why the loss of SIGIRR leads to uncontrolled inflammation in AMD, and whether the development of AMD can be delayed or halted by enhancing SIGIRR expression through gene therapy.
Advanced molecular biology and immunology techniques will be used in cell culture and animal models to investigate how SIGIRR expression changes in normal and AMD eyes. Finally, gene therapy will be used to test whether AMD related inflammation and retinal damage can be prevented or reduced by over-expressing SIGIRR in the retina.
The study will provide essential evidence to establish the role of SIGIRR in macular inflammation and inflammation-mediated macular damage in AMD. It will demonstrate whether targeting SIGIRR by gene therapy is beneficial in AMD, which may lead to the discovery of novel biomarkers to predict the progression of the disease, and effective approaches to treat dry AMD.
One molecule that can turn off the inflammatory process is called SIGIRR. Researchers have found that eyes donated from dry AMD patients have less SIGIRR when compared with eyes from healthy donors. Mice without SIGIRR developed dry AMD-like disease in the eye. The results suggested that insufficient SIGIRR may be a key factor for uncontrolled inflammation in AMD. Therefore, enhancing SIGIRR expression could be a novel approach for immune therapy.
Researchers aim to understand why the loss of SIGIRR leads to uncontrolled inflammation in AMD, and whether the development of AMD can be delayed or halted by enhancing SIGIRR expression through gene therapy.
Advanced molecular biology and immunology techniques will be used in cell culture and animal models to investigate how SIGIRR expression changes in normal and AMD eyes. Finally, gene therapy will be used to test whether AMD related inflammation and retinal damage can be prevented or reduced by over-expressing SIGIRR in the retina.
The study will provide essential evidence to establish the role of SIGIRR in macular inflammation and inflammation-mediated macular damage in AMD. It will demonstrate whether targeting SIGIRR by gene therapy is beneficial in AMD, which may lead to the discovery of novel biomarkers to predict the progression of the disease, and effective approaches to treat dry AMD.