Retinal disorders are considered an appropriate target for cell therapy, and the combination of unique anatomic and clinical features render the eye particularly favorable for clinical testing.

Photoreceptor death is the final irreversible event in many blinding diseases, and even a modest reduction in the rate of photoreceptor loss by a neuroprotective approach may lead to significant prolongation of useful vision. This strategy may be particularly relevant in the setting of the rate of changes observed in the natural history of AMD (Luther, 1982). Transplants to slow the loss of existing neurons (i.e., photoreceptors) in the degenerating retina may be the first useful method for maintaining some degree of vision (Vugler, 2007). In many ways, the eye is an ideal organ in which to assess transplant success because objective techniques are available to monitor visual function and anatomy.

The unique attributes of the eye particularly facilitative of testing cell-based neuroprotective interventions are as follows:

• Retinal degeneration is characterized by discreet and small anatomic regions of disease eminently scalable for rescue by cell transplantation.
• The subretinal space is relatively immune privileged and consequently is potentially permissive to long-term allograft survival.
• Subretinal surgery is a minimally invasive vitreo-retinal technique and can be performed as an out-patient procedure.
• Measures of visual acuity, direct fundus examination, retinal electrophysiology, and in vivo retinal imaging offer objective, noninvasive methods of retinal function and outcomes.
• Outcomes from the treatment eye can be compared with outcomes from the untreated fellow eye. 
The advantages of cell-based neuroprotective approaches for GA AMD are:
• GA AMD has no curative therapy and represents an area of significant unmet need
• The final common pathway of vision deterioration in GA AMD is photoreceptor loss
• The rate of progression in GA AMD affords the prospect of early intervention and subsequent rescue of degenerating photoreceptors and possible slowing or stabilization of the rate of vision loss
• Cell-based approaches targeting neuroprotection of photoreceptors do not require the complex phenotype recapitulation, integration, and attachment expected by photoreceptor and RPE replacement strategies
• Neurotrophic factors potentially delivered by cell transplantation circumvent the obstacle posed by the blood-retinal barrier, which impedes access of intermittent systemically administered large molecules to the neural retina
• Proof of concept for neuroprotection of host photoreceptors by subretinal transplantation using various tissue and cells has been established in non-clinical studies
• Previous clinical trials have demonstrated the feasibility and procedural safety for allogeneic subretinal transplantation in subjects with retinal degeneration

Based on the results of non-clinical studies in the dystrophic RCS rat model (Section 4.3), subretinal transplantation of hNSC represents a candidate neuroprotection strategy to prevent or slow photoreceptor loss secondary to GA AMD