**4. Potential therapeutics for AMD**

There are many studies that have evaluated potential therapies for non-exudative and exudative AMD. Along with vitamin supplementation, there are three main classes of therapies being investigated: antibody, gene, and cell-based therapies.

Aside from the successful anti-VEGF therapies, antibodies targeting the complement pathway show some promise. Because activation of the alternative complement pathway contributes to AMD pathology, antibodies targeting components of this pathway, such as C3 and C5, may attenuate inflammation and damage to the retina by reducing complement mediated cell lysis [53, 54].

Gene therapy involves introducing genetic material, typically a viral vector, into tissues of interest to replace the blueprint of a protein product. The most used viral vectors are adeno-associated viral vectors due to their lower immunogenicity and extended duration of gene expression [54].

Another way to treat AMD is through cellular therapy which works by replacing a protein product, like gene therapy; however, instead of replacing the genetic code, the cells that produce the protein of interest are replaced or supplemented. Cellular therapy allows for the replacement of dead or diseased tissue with healthy tissue. For AMD, this typically involves replacement of the RPE. Replacement of neural retinal tissue is challenging as it relies on the reestablishment of neural connections. In contrast, the RPE does not have neural connections, but serves to maintain healthy photoreceptors by providing nutrients and removing waste products. For these reasons, the RPE is currently the primary target of cell-based therapy for AMD [54]. Another promising cellular therapy for exudative AMD is replacement of the choroidal endothelial layer as this may prevent neovascularization [55]. However, there are many challenges associated with the delivery of cell-based therapy such as immune rejection, high rates of tumor formation, and differentiation into unintended cell types. Previous studies have shown the dangers of using stem cell therapy in the treatment of AMD citing complications like IVT fibrosis and tractional retinal detachment [56]. Furthermore, the timing of RPE transplant is critical to its success. It must be performed early enough so that the underlying retinal cells can still be salvaged; however, performing the therapy too early runs the risk of complications from prepathological intervention [54].
