A new drug therapy for age-related macular degeneration
- Grant holder: Dr Xinhua Shu, Reader in Biomedical/Vision Sciences, Department of Biological and Biomedical Sciences
- Institution: Glasgow Caledonian University
- Grant award: £69,995
- Start: August 2018
- End: August 2021
Why is this research needed?
Age related macular degeneration (AMD) is the leading cause of severe and permanent sight loss in the UK, and in the developed world. This progressive disease damages the macular: the part of the eye that is responsible for our central, detailed, and much of our colour vision. A poor understanding of exactly what causes the macula to become damaged means that AMD is currently incurable and, for the most part, untreatable.
Dr Shu’s project focuses on one of the most prominent early indicators of AMD, in order to determine whether treating this key symptom can halt the progress of disease in patients, and save their sight from deteriorating.
In the early stages of AMD, fatty deposits build up between layers in the retina known as the retinal pigment epithelium (RPE) and Bruch’s membrane. The RPE is a single layer of highly pigmented cells that performs many critical functions, including supporting retinal photoreceptors, which convert light into signals that are sent to the brain, enabling us to see. Bruch’s membrane lies underneath the RPE. The fatty deposits, known as drusen, which accumulate between these layers, can also build up between the RPE and the photoreceptors.
Drusen contain a variety of fatty substances, including cholesterol. The source of the cholesterol is thought to come from photopigment-containing discs, found in the photoreceptor cells. In a healthily functioning retina, the RPE cells break down and digest these discs. It is thought that excess cholesterol should move from the RPE into the Bruch’s membrane, from where it is returned to the liver through a process called reverse cholesterol transport (RCT), before being excreted as bile. It is further supposed that fatty deposits found in the retinas of people with AMD could be due to dysfunctional RCT, especially as several RCT-related genes have been shown to be predictive risk factors for AMD.
What is the aim of the project?
In a recent study, Dr Shu’s team demonstrated that a protein called TSPO is involved in promoting cholesterol removal from RPE cells. Furthermore, if the gene that produces TSPO is missing, the removal of cholesterol is significantly decreased, resulting in an accumulation of deposits inside the RPE cells.
Dr Shu’s project is exploring whether drugs designed to target the TSPO producing gene can stimulate the removal of cholesterol from the RPE, and supress the formation of fatty deposits.
How will this research help to beat sight loss faster?
The knowledge gained through this project will aid the development of new drugs that could be used to treat AMD at an early stage to halt the progression of the disease, thereby preventing sight loss.
You can find more about the causes and symptoms of AMD here.
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