Silmara de Lima, PhD

I have been studying RGC survival and axon regeneration in the optic nerve injury model, since 2007, when I started my Master in Brazil, and continued studying this topic during my PhD training, which started in Brazil and continued at Boston Children’s Hospital/Harvard Medical School. Dr. Larry Benowitz, one of the leaders in the field of optic nerve regeneration, was my mentor for a major part of my PhD training and we showed that retinal ganglion cells (RGCs) can regenerate their axons along the full-length of the optic nerve, enter the brain, reach visual targets, and become myelinated. In another study we demonstrated that regenerating axons could reassemble important domains that are responsible for the propagation of action potential, the signal that travels from the retina to the visual targets in the brain. Our work and the work of others have helped advance the field of regenerative medicine of the visual system. To study RGC survival and regeneration we used the optic nerve crush model, an acute lesion that causes dramatic RGC loss and massive axon degeneration in a short time span. In the past few years, I have been studying RGC survival and axon degeneration in a mouse model that phenocopies the formation of optic pathway gliomas (OPG) seen in patients with the genetic disorder Neurofibromatosis type 1 (NF1). In this model, RGC loss and axon degeneration progress slowly, making the NF1-OPG model a promising alternative to study mechanisms and potential targets for neuroprotection of RGCs.