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Prof James E Morgan 


Staff Photos
Position:Professor in Ophthalmology, Consultant Ophthalmologist

Telephone:+44 (0)29 2074 3222 / 2074 4970
Fax:+44 (0)29 2074 3222
Extension:76344
Location:Room 2.37, Maindy Road

Research Interests

My research is aimed at understanding the structural and cellular changes occurring at the level of the optic nerve in glaucoma using clinical and laboratory based techniques. Glaucoma is one of the most common causes of vision loss in the UK population, affecting up to 2% of the population as a whole. Classically, it is associated with increased intraocular pressure, which causes the death of retinal ganglion cells and results in a slow and, if untreated, progressive loss of vision. In most cases, peripheral vision is lost first and is usually asymptomatic. By the time a patient notices restriction of visual field, advanced damage may have occurred to the optic nerve that is usually irreversible. Treatment is aimed at the reduction of eye pressure (intraocular pressure) to prevent this vision loss. Usually, this is achieved using eye drops although, in some cases, surgery or even laser treatment may be required. One of the key problems is in identifying the disease in its earliest stages and in detecting the first signs of retinal (optic nerve) damage.

As a consultant ophthalmologist, I run a glaucoma service at the University Hospital of Wales. I currently chair the Expert Working Group for the development of shared care glaucoma in Wales where we are working to develop the role of virtual clinics for the community care of patients with diagnosed glaucoma.

Clinical studies

These are based at the Retinal Imaging Laboratory and are directed at the quantification of structural optic nerve changes in the early stages of glaucoma. Since these precede the development of visual field changes as detected using clinical perimetric techniques, their detection should enable early disease diagnosis and improve the long-term prognosis for the patient. We are currently assessing the value of digital stereoviewing in the quantification of these nerve head changes. In addition, we are assessing the value of other imaging modalities such as OCT in the determination of optic nerve head changes that occur in early glaucoma.

Retinal ganglion cell transfected with plasmid coding for GFP. Retinal Explant preparation after 24 hours in culture.

Retinal ganglion cell transfected with plasmid coding for GFP. Retinal Explant preparation after 24 hours in culture.

Using a variety of in vivo and in vitro models of glaucoma, my group is investigating the mechanisms of retinal ganglion cell death in glaucoma. There is good evidence that these cells undergo a prolonged period of atrophy and remodelling prior to cell death, which is manifest as shrinkage and pruning in the cell body and dendritic processes. These changes will reduce the efficiency with which these cells can detect visual signals but also suggests that this damage could be reversed. We use techniques such as biolistics transfection to see if the overexpression of genes that might be beneficial for retinal neurons can result in cell rescue (Insert figure here).

We are collaborating with Bruce Caterson in the School of Biosciences to determine the role of extracellular matrix and the perineuronal net in limiting the extent to which retinal ganglion cells can recover from injury.

We are developing techniques for the early detection of these changes using imaging techniques such as OCT. We are currently investigating the possibility that OCT can detect optical signal associated with sub-cellular changes that are the earliest changes that occur prior to cell death. These studies are being undertaken with Wolfgang Drexler and Boris Povazay in the Biomedical Imaging Group.