Seven new PhD studentship awards for 2015
Fight for Sight has awarded seven new PhD studentships in eye research for 2015.
The awards, which total almost £700,000, will fund a wide range of projects, from developing cell replacement therapy to understanding sight loss from head injury and using new technology to pinpoint the earliest stages of cataract formation.
We award our prestigious studentships each year to encourage some of the UK’s best young science graduates to pursue a career in eye research. The awards give the students a chance to spend three years at a world-class institution, doing cutting-edge research.
Marianne Piano is a young researcher who has just completed a 3-year Fight for Sight PhD studentship under the guidance of Professor Anita Simmers at Glasgow Caledonian University. Marianne has been using 3D monitors, stereo ‘shutter’ glasses and eye-tracking technology to study distorted vision in people with amblyopia (or ‘lazy eye’).
Helping people make the most of their vision
“My chosen career revolves around helping people to make the most of their vision,” said Marianne. “None of it would have been possible without Fight for Sight’s funding and support. Thank you.
“I'm now using my research skills gained during the studentship to coordinate a randomised controlled trial looking at video game training to improve vision in children with residual amblyopia after treatment.”
Dr Dolores M Conroy is Fight for Sight’s Director of Research. She said: “I’m very encouraged to see such a strong set of research projects for our 2015 PhD studentships. They include fundamental work to understand sight loss at the genetic and molecular levels alongside research that could benefit patients in the clinic in the near future.
A strong UK community of eye researchers
“I’ve no doubt we will see some important advances in eye research as a result and that we will welcome a new group of talented research students such as Marianne into the field to sustain a strong community of eye researchers in the UK.”
The studentships will start with the academic year in October. You can read a brief summary of the seven projects below.
2015 PhD studentship summaries
Supervisor: Dr Rachael Pearson, UCL Institute of Ophthalmology
What stops transplanted cells from reaching the right part of the eye?
Cell replacement therapy is an exciting idea that could become important way to treat blindness due to loss of the light-detecting cells in the eye (the ‘photoreceptor’ cells). For it to work, young photoreceptors need to move into the right place in the retina (the part of the eye that contains photoreceptors) where they can link up with other cells and start working.
Unfortunately, when photoreceptors are lost they can be replaced with scar tissue, which forms a barrier that makes it hard for any new cells to move into position. The research team have found that fewer than 1 in 10 cells make it through when transplanted into animals with loss of photoreceptors.
But they have also found that high levels of molecules called ‘chondroitin sulphate proteoglycans’ are linked to low success rates. Whenever they find low levels of these molecules, more transplanted cells succeed. So in this study the student will aim to confirm whether and how these molecules interfere with transplantation.
Supervisor: Professor Andrew Webster, Moorfields Eye Hospital
Which genes are key to developing the eye’s central vision detector?
The macula is found at the centre of the light detecting region of the eye, known as the retina. The macula is responsible for central vision and can perform fine visual tasks such as reading and recognising facial expressions. Although research has discovered lots about what goes wrong in age-related macular degeneration, we don’t yet know much about how the macula develops in humans.
In this project the research team will be studying the genetics of three rare inherited eye disorders that lead babies to be born with damaged maculae. At the moment we don’t know exactly which genes or what type of ‘spelling mistake’ (genetic mutation) are involved. But the team has a large group of patients with these disorders, so the student will be pulling together their genetic data and comparing it to DNA from previous animal work and from stem cells taken from patients.
The aim is to find the genes that will allow families to be given a specific diagnosis and to understand more about how future drugs might target the macula.
Supervisor: Dr Patrick Yu-Wai-Man
How do faults in the WFS1 gene lead to cell death in Wolfram syndrome?
In Wolfram syndrome the cells that carry visual signals from the eye to the brain (known as retinal ganglion cells) die off over time. People with Wolfram syndrome start to lose their sight as young children and are usually registered blind by mid- late adulthood. At the moment there is no treatment but we do know that the syndrome is linked to a fault in the gene WFS1.
Previous research suggests that WSF1 is involved with the way that cells produce the energy they need to survive and work. In this project the student will study some of the processes that are known to lead to cell death, such as poor energy production, to find out exactly how WSF1 is involved.
Supervisor: Dr Yalin Zheng, University of Liverpool
Automatic computer screening for diabetic eye disease
Diabetic eye disease is leading cause of blindness in working age people in the Western world. Not everyone with diabetes will develop diabetic eye disease but in order to catch it early people with diabetes are invited to have the back of their eyes photographed each year.
Of the 2.5 million people with diabetes in England, 1.9 million were screened in 2011-12. At the moment, the pictures are checked by people trained to grade them on whether they show diabetic eye disease and at what stage. This takes time and is expensive.
In this project the student will develop an automatic way to find and classify the condition using a computing technique known as deep learning. They will use around 4,000 images to teach the computer which features turn up in the images in people with diabetic retinopathy (and aren’t there in people who don’t have the condition). They’ll also teach the computer to grade the images and will finally test the computer against human graders, to find out how well it performs. If successful, the team will look for extra funding to turn the software into a tool that can be used in the clinic.
Supervisor: Dr Zubair Ahmed, University of Birmingham
What happens to cells in the optic nerve after an indirect head injury that affects sight?
About 8000 people each year in the UK lose their sight after an injury to the head. Sometimes, the optic nerve (which carries visual signals from the eye to the brain) is crushed or cut directly. But more often, a head injury or eye injury leads indirectly to the optic nerve cells dying.
So in this project the student will try to find out more about how a blunt blow or blast injury might lead to cell death. They will compare what happens to retinal ganglion cells (which make up the optic nerve) after different types of injury. They’ll also try to find out whether blocking a particular chain of chemical events inside the cells can prevent them from dying.
If so, the team will seek funds at the end of the project to begin clinical trials. In addition to people with sight loss from head trauma, the project could potentially help people with glaucoma.
Supervisor: Dr Sergi Garcia-Manyes, King’s College London
Watching cataracts unfold
Age-related cataract (where the clear lens at the front of the eye slowly becomes cloudy) is responsible for almost half of the world’s blindness. Cataracts happen when proteins in the lens stop working normally and start to build up. Research has shown that this build-up is triggered by ‘misfolding’ proteins. Usually, proteins in the body need to be folded into the correct shape in order to work.
In this project the team will use a new technique known as ‘single molecule force-clamp spectroscopy’ to study each step individual protein molecules take in the process of unfolding. The aim is to pinpoint the exact step at which folding starts to go wrong and to track what happens afterwards. Results from the project will help us understand, for the first time, how protein misfolding in the lens begins. This is a vital step towards developing a non-surgical treatment to prevent or delay cataract.
Supervisor: Dr David Kavanagh, Newcastle University
C9: A new genetic risk factor for AMD
Age-related macular degeneration (AMD) causes people to lose their central vision. Several studies have linked the risk of getting AMD to certain genetic changes that affect what’s known as the ‘complement system’. This is part of the body’s defence against bacteria and viruses, but if it goes wrong it can turn on the body’s own cells.
The research team has recently found a new genetic link to a protein called C9, which is part of the complement system. In this project they will study blood and cell samples from patients with AMD to find out whether C9 is overactive. They will also try to develop an antibody test that would identify which patients could benefit from new drugs that stop the complement system from becoming overactive.
At the end of the project the team aim to have a test that can identify people at risk of AMD due to C9 and the data needed to develop targeted drug treatments.