A World Health Organization 2001 report stated that

between 40 and 45 million people worldwide are blind. A significant portion of those have some form of optic nerve degeneration [1,2]. Although the problem is immense, thera-peutic approaches to regenerating damaged optic nerves lag substantially behind those used for other types of ocular disease. In addition, animal models currently available for developing new therapeutic strategies suffer from several serious limitations [1]. We recently developed a robust genetically engineered adult mouse model of retinal ganglion cell (RGC) loss and optic nerve degeneration based on genetic ablation. We took advantage of the Pou4f2 gene, which is essential to RGC differentiation and is expressed in RGCs throughout life. Adult mice were generated whose genomes harbored a conditional Pou4f2 allele containing a floxed-lacZ-stop-dta cassette and a CAGG-Cre-ER transgene (Dta mice). When mice at different ages were administered tamoxifen by intraperitoneal injection, the result was rapid RGC loss, reactive gliosis, progressive degradation of the optic nerve over a period of several months, and visual impairment [3]. Although the efficiency of the toxin-mediated cell death was high and completely ablated all Pou4f2-expressing RGC, the retinas maintained their structural integrity even in two-year-old mice [3]. The Dta mouse model is particularly relevant for RGC death and optic nerve degeneration in human retinal pathologies, where the degeneration of non-RGC types does not typically occur until advanced stages of pathogenesis