**6. Conclusion**

AMD is a complex, multifaceted disease that is becoming more prevalent in the aging population. Animal models provide insight into our current understanding of disease pathophysiology including an interplay of oxidative stress, inflammation, dysregulated antioxidants, lipid metabolism, and angiogenesis juxtaposed with genetic and environmental risk factors, the greatest of which are aging and cigarette smoking. Mice are the most used animal models and have provided information such as the roles of antioxidants and inflammation in AMD pathophysiology. Mice also provide excellent polygenic models which may better represent the complex pathology of AMD. Although other animal models, such as rabbits, have been helpful, NHP eyes are the most like human eyes making them an invaluable resource; however cost and ethical issues limit their widespread use.

After disease progresses to exudative AMD, there are several FDA-approved treatments such as bevacizumab, ranibizumab, aflibercept, and most recently brolucizumab that block members of the VEGF family of proteins. Through the AREDS 2 study, vitamin supplementation consisting of 500 mg vitamin C, 400 IU vitamin E, 10 mg of lutein and 2 mg of zeaxanthin, 80 mg of zinc (zinc oxide), and 2 mg of copper (cupric oxide) can slow the progression to advanced AMD. Although treatment options are currently limited, there are studies in various clinical phases evaluating potential therapies for both non-exudative and exudative AMD. Three main classes under investigation are antibodies, genes, and cell-based therapies. The virtuous cycle of bidirectional translation, along with the use of improved animal models, enhances our understanding of AMD pathophysiology and opens the doors to innovative treatment options.
