Myopia, or nearsightedness, is the only cause among the top five causes of blindness in the world that remains completely untreatable and has reached epidemic proportions. Characterized by a thin choroid layer and increased axial eye length, myopia develops when the eye continues to grow so that images of objects seen in the distance become in focus in front of the retina rather than at the retina itself. This study aims to find a means to prevent the progression of myopia from its onset during early childhood, and help the eye return to a length closer to emmetropia, a process in which the eye stops growing when objects are in maximal focus at most distances. Specifically, we developed and tested a prototype blurry lens (eye glasses) to see if it could serve as a potential means to decrease the axial length of the eye, increase the thickness of the choroid layer, and ultimately help prevent the progression of myopia. Subjects were required to wear glasses in which the left eye was UV irradiated with a blurry pattern and the right eye served as a self-regulated control. The choroid layer was measured in pre and post-treatment sessions using OCT (optical coherence tomography) imaging of the retina and choroid via a Rowland RETImap OCT machine and standard regression analyses. Results show a significant increase in the choroidal thickness and decrease in the axial length of the left eye compared to the control and baseline measurements, along with a change in retinal morphology. Our study suggests that the eye experiences signals that modulate its axial length in response to myopic stress. Thus, the blurred lenses were an effective means to prevent the progression of myopia because they brought about similar changes in axial length and choroidal thickness changes as seen in emmetropic conditions.

 The human retina is a complex, post-mitotic tissue where the visual process is initiated. More specifically, it begins when photoreceptor cells absorb light. When these photoreceptors are lost due to damage or disease, irreversible loss of vision results. One potential therapy is cell transplantation of newly generated photoreceptors to replace these lost cells. Regardless of where these stem cells are derived from a common obstacle faced is the proper integration of the transplanted cells with the surrounding native cells. Here we investigate wheat germ agglutinin (WGA) as a potential tool to detect proper integration of photoreceptors by exploiting WGA’s known capacity to serve as a transsynaptic tracer among integrated neurons. Recombinant adeno-associated viruses (rAAVs) were generated encoding WGA conjugated to red flourescent proteins (DsRed) under either a ubiquitous (CMV) or photoreceptor specific (IRBP) promoter.The rAAV genomes also contained another fluorescent protein (GFP) to identify infected cells. Negative controls for transsynaptic movement (where WGA is absent) were included. These rAAVs were delivered via subretinal injections in 2-3 months old mice. The murine eyes were then harvested after 4 days, 2 weeks, and 3 weeks post injection and examined for red florescence, indicating transsynaptic movement. In an attempt to increase transsynaptic signaling, mice were housed in constant darkness and compared to their light-adapted controls. We have been able to show modest WGA-dependent transsynaptic signaling from the infected photoreceptors to their second- and third-ordered neurons (bipolars and ganglion cells, respectively). These transsynaptic signals appear to occur from robust cellular expression of WGA and were not affected by the housing conditions for the mice. These results support an accumulation requirement for transsynaptic movement. Further investigation into enhancing the WGA expression in photoreceptors are needed so that it could become a more powerful tool to examine the integration capacities of transplanted cells for future transplantation studies.