Specifically, the aims of recent projects were to determine whether
axonal cytoskeletal disruption, transport abnormalities, and electrophysiological dysfunction occur prior to RGC death in experimental glaucoma (rodent and non-human primate models) and whether some of these phenomena are detectable by clinically - applicable means.
We aim to close this gap by implementing a novel assay to simultaneously assess the integrity of
the axonal cytoskeletal structure (using electron microscopy) and a functional (physiological) correlate of healthy cytoskeletal structure, namely active axon transport, within individual RGC axons at an early stage of experimental glaucoma.