- Glaucoma, neuroprotection
- Regulation of ganglion cell death and the role of Bax
- Epigentic changes in apoptotic ganglion cells leading to gene silencing
- Identification of ganglion cell death susceptibility alleles
T32 Training Area:
Development and Diseases of the Anterior Segment
Physiology, UW Comprehensive Cancer Center, Institute on Aging, Eye Research Institute
- BS 1983, University of Victoria, British Columbia, Canada
- PhD 1987, University of Calgary, Alberta, Canada
- Postdoctoral Fellowship, 1987-90, California Institute of Technology, Pasadena, CA
Glaucoma is one of the leading causes of blindness world-wide. Although an increase in intraocular pressure is often associated with this disease, it is marked by the progressive death of retinal ganglion cells. Previous studies by my laboratory and others have shown that ganglion cell death occurs by a mechanism that is characteristic of apoptosis – a form of programmed cell death that is regulated by a successive activation of genes from within the dying cell. Hypothetically, neuronal cell death can be blocked or prevented by agents that interrupt key biochemical pathways that are controlled by these genes. This form of treatment, termed neuroprotection may provide important avenues of therapy for many neurodegenerative disorders which includes glaucoma.
My laboratory studies some of the earliest events that occur in retinal ganglion cells during the cell death process. For these studies we make use of mice lacking genes critical for the cell death process. Our current focus is on epigenetic changes that lead to silencing of normal gene expression well in advance of the committed step in the apoptotic pathway.