Member of Brain Research Centre
Member of Graduate Program in Neurosciences
Member of Graduate Program in Cell and Developmental Biology
Associate Member of Cellular and Physiological Sciences
Ph.D.University of California, San Diego (USA)
For a description of the current research studies in Dr. Matsubara’s Lab, click here.
Highlights of Dr. Joanne Matsubara’s research can be seen here: “Focusing on Eye Disease” International Innovation: Healthcare August 2013 (Research Media, UK pp 36-39, ISSN 2051-8501)
Age-Related Macular Degeneration (AMD):
AMD is a major cause of blindness observed among the elderly worldwide. At present, there are an estimated one million individuals in Canada living with AMD, and by 2013 this number is expected to double. Currently, there are no treatments for dry AMD, which accounts for over 90% of the AMD patients, and there is only one approved treatment for slowing, but not preventing, vision loss in the wet form of AMD (10% of the AMD patients).
In AMD, a cell type in the back of the eye, the photoreceptor cell (PR), becomes unhealthy and eventually dies. Once these cells die, they are never replaced, and blindness occurs. Fortunately, neighboring cells, the retinal pigment epithelial cell (RPE), support and nurse the photoreceptor cells, so that they stay healthy. The problem in dry AMD is that these nurse cells, the RPE, also become unhealthy and lose their ability to nurse the photoreceptor cells, and thus cause blindness.
The early stage of dry AMD is identified by the presence drusen, extracellular deposits located between the retinal pigment epithelium (RPE) and Bruch’s membrane. The disease progresses to late stage geographic atrophy (GA) and is characterized by high drusen load, RPE dysfunction and photoreceptor death. Many risk factors, such as genetics, drusen load and aging, play important roles in the pathogenesis of AMD. Studies from our lab have shown that these risk factors are associated with an imbalance in systemic and local retinal inflammatory mediators hypothesized to promote disease progression.
Our premise is that genetics, drusen and aging, three risk factors for AMD, channel their effects into two cellular processes: complement cascade and inflammasome activation. Our lab studies the effects of complement cascade and inflammasome activation on the RPE cell in cell culture and animal models of AMD. Here is an overview of our studies. Full references can be found under publications.