Fletcher laboratory: Visual neuroscience

Research Overview

View Professor Fletcher's latest publication listing here

The Visual Neuroscience laboratory is interested in:

  • Why photoreceptors die during retinal degeneration, including retinitis pigmentosa (RP) and Age-Related Macular Degeneration (AMD)
  • The role of glia and microglia in retinal diseases such as Diabetic Retinopathy (DR)
  • Ways of replacing lost photoreceptors or slowing photoreceptor death in inherited retinal degenerations

Diseases of the Retina that Cause Blindness

Retinal diseases are a major cause of blindness in the Western world. Few treatments are currently available, largely because the underlying mechanisms of disease are not well understood.

Our laboratory studies two broad classes of retinal disease:

1. Retinal degenerations, including Age-Related Macular degeneration

Retinal degenerations are a family of hereditary diseases that cause a gradual loss of photoreceptors leading to blindness. These diseases occur in around 1:5500 people, but 1:50 are carriers. We are examining the mechanisms of photoreceptor death and whether specific treatments ameliorate or slow the loss of photoreceptors. Understanding how photoreceptors die is of relevance to diseases such as Age-Related Macular Degeneration (AMD), which is one of the leading causes of blindness especially in older people. Photoreceptor death and abnormal growth of blood vessels into the retina are major contributors to blindness in this disease. We use pre-clinical models to understand the underlying mechanisms involved and whether treatments slow the progression of disease. Our ultimate goal is to develop ways of slowing photoreceptor death and also to investigate ways of replacing lost photoreceptors.

2. Retinal vascular diseases, including Diabetic retinopathy

Diabetes affects 3.8% of the population of Australia, at an annual cost of AUS$1 billion dollars. Diabetic retinopathy is a common complication associated with diabetes and is the leading cause of blindness in those under 65 years of age. Some 10% of all diabetics experience vision threatening retinopathy. One of the major reasons for vision loss is the growth of new blood vessels in the retina (neovascularization). Although a great deal of attention has focussed on the vascular changes associated with diabetes, it is now emerging that changes in neuronal, glial and microglial cell function often occur prior to overt vascular abnormalities. Understanding the link between microglial, glial cell dysfunction and changes in vasculature is vital for gaining a better understanding of the pathogenesis of diabetic retinopathy. The major thrust of our work is understanding the changes in the retina that lead to neovascularization. We also examine whether novel treatments prevent or slow vision loss.

Staff

Dr Ursula Greferath, Senior Research Officer

Dr Kirstan Vessey, Senior Research Officer

Dr Andrew Jobling, Senior Research Officer

Dr Joanna Phipps, ARC DECRA Fellow

Dr Alice Brandli, ARC DECRA Fellow

Gene Venables, Research Assistant

Satya Gunnam, Research Assistant

Stefanie Dudczig, Research Assistant

Michael Dixon, PhD student

Anna Wang, PhD student

Quan Findlay, PhD student

Josephine Wong, PhD student

Vanco Hristov, PhD student

Pialuisa Quiriconi, Honours student

Collaborators

Professor Michael Kalloniatis, Centre for Eye Health and Dept. Optometry, UNSW

Professor Richard Kramer, Molecular & Cell Biology, UC Berkley

A/Professor Bang Bui, Department of Optometry and Vision Sciences, University of Melbourne

A/Professor Botir Sagdullaev, Department of Ophthalmology, Burke Neurological Institute, Weill Cornell Medicine

Funding

National Health & Medical Research Council of Australia
Australian Research Council
Retina Australia
American Health Assistance Foundation
Commercial contracts

Research Opportunities

This research project is available to Masters by Research, Honours, Master of Biomedical Science students to join as part of their thesis.
Please contact the Research Group Leader to discuss your options.