Dr. Friedlander studies interactions between neurons, glia, and endothelial cells in the retina. Referred to as the “neurovascular unit,” these cells work together to ensure that the dynamic metabolic needs of neurons are met.
MacTel affects the cells that make up the neurovascular unit: neurons, glia, and endothelial cells. The result is vision loss and vascular changes. Histopathology and clinical data suggest that MacTel affects neurons and glia before it causes changes to blood vessels. Dr. Friedlander’s group is working to understand how photoreceptors, endothelial cells, and Mueller glia functionally interact. His group has discovered that photoreceptors can initiate a cascade of events within the neurovascular unit that results in vascular maintenance.
Dr. Friedlander has a long-standing interest in the fundamental biology of retinal angiogenesis, one of the pathological features of MacTel. His group uses transgenic mice that exhibit vascular features characteristic of MacTel to study pathological retinal angiogenesis. They have used these models to understand how the retina stabilizes and maintains its vasculature.
In addition to studying the cells and molecules that maintain the vasculature, Dr. Friedlander’s lab also identifies compounds that maintain photoreceptors in the retina. Inosine is one such neurotrophic compound that his group studies. Neurotrophic agents have a protective effect on the retina, and his group is working to understand their activity and optimize their delivery.
Dr. Friedlander’s work is based on proof-of-concept evidence that vascular repair and neurotrophism can prevent photoreceptor atrophy characteristic of MacTel. Central to these studies is the neurovascular unit. His group is continuing to determine how photoreceptor/endothelial cell/Mueller glia crosstalk is central to retinal homeostasis in order to prevent vision loss and vascular changes characteristic of MacTel and other neurodegenerative diseases.