Sub-retinal blood vessel damage and the development of dry AMD

Brief Lay background

Age-related macular degeneration (AMD), causes loss of central vision because of damage to the macula – a tiny collection of light-sensitive cells found within the retina at the back of the eye.

AMD is the most common cause of permanent and severe sight loss in the UK, affecting around 600,000 people – this number is expected to more than double by 2050.

What problem/knowledge gap does it help address

People with the early stages of AMD will usually have few symptoms – but those with later stages will experience severe sight loss that hugely affects their quality of life.

Dry AMD is the most common type of age-related macular degeneration. It is caused by a build-up of waste and thinning of the retina, which causes it to function less effectively.

Unfortunately, there are no effective treatments that can help slow down or prevent dry AMD from progressing to late-stage disease (also called ‘geographic atrophy’).

Aim of the project

To improve understanding of the role of age-related damage to a network of specialised blood vessels (called the choriocapillaris) underneath the retina in the development of dry AMD – and to investigate potential ways to boost the capacity of these blood vessels to repair themselves and help maintain the health of the retina.

Key procedures/objectives

1. Study the role of a key biological mechanism in maintaining the choriocapillaris during health and disease.
2. Understand the effects of treating certain cells (which have the potential to repair damage to the choriocapillaris) with a molecule called APC.
3. Explore the potential of using APC as a treatment approach for repairing damage to the choriocapillaris.

Potential impact on people with sight loss

Patients with early-stage dry AMD could ultimately benefit from exciting new treatments that can help prevent the disease from progressing to later stages – helping to slow down or stop sight loss and dramatically improving their quality of life.