Using pre-clinical models of acute and chronic optic nerve damage, Dr. Adriana Di Polo’s lab seeks to identify molecular cues that control retinal ganglion cell survival in the injured eye. We are also investigating the role of reactive glia and vascular deficits in glaucomatous neurodegeneration.
NEURONAL SURVIVAL AND REGENERATION
Dr. Adriana Di Polo’s laboratory seeks to identify molecular cues that control retinal ganglion cell survival and regeneration in the injured eye. Using pre-clinical models of acute and chronic optic nerve damage, we are currently investigating signals that regulate retinal ganglion cell death, dendrite retraction and regrowth, axon degeneration, synaptic loss and dysfunction. Our laboratory has been actively involved in pre-clinical development of compounds currently in clinical trials for ophthalmological applications. The goal of Dr. Di Polo’s laboratory is to use this knowledge to develop clinically-viable strategies to enhance retinal ganglion cell protection and regeneration in glaucoma.
ROLE OF REACTIVE GLIA
Glial cells play critical roles in the maintenance of retinal function. Recent data demonstrate an important neuroinflammatory component in glaucoma characterized by reactive gliosis and upregulation of proinflammatory cytokines. We are actively investigating how reactive glia contribute to retinal ganglion cell damage in glaucoma.
The retina is amongst the most metabolically active tissues in the body and requires a precise regulation of blood supply to meet its high oxygen demand. Vascular deficits have been proposed to contribute to retinal ganglion cell death and glaucoma progression. We seek to understand the mechanisms that lead to neurovascular dysfunction in glaucoma.