Grant: Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships

FOXC1 is a protein that is necessary for the normal development of the eye. When there are mutations in FOXC1, patients develop Axenfeld-Rieger syndrome. These patients have an increased risk to develop glaucoma, which is one of the leading causes of blindness in the world. Despite intensive research over the years, the mechanism of how a patient develops glaucoma remains largely unknown. Our eyes are subjected to many kinds of stress everyday. These stresses include exposure to light and even changes in body position. Usually, the cells that make up our eyes have various mechanisms to efficiently respond to stress. However, as we age, the cells are less efficient in dealing with these stresses. An inability to efficiently respond to stress has been suggested to promote the development of glaucoma. My research will examine how FOXC1 dysfunction affects the function of other downstream genes that are important in responding to stress. We believe that the cells in patients with Axenfeld-Rieger syndrome are not as efficient in coping with various kinds of stresses and this is why many of them develop glaucoma very early on in their lives. Understanding how FOXC1 mutations can cause glaucoma will not only provide insight into developing treatments for people with Axenfeld-Rieger syndrome. Rather, this will be the first step towards developing effective treatments for all people with glaucoma. Finding ways to prevent the decline in efficiency of a cell's ability to respond to stress will prevent or in the least, delay the onset of glaucoma. Although glaucoma is a non-life-threatening disease, it is still a devastating disease because it severely decreases the quality of life of patients. My research focuses on deciphering the molecular mechanisms of this very common disease. However, the ultimate goal of my research is to promote the development of treatments that will improve the quality of life of patients with glaucoma.