*2.2.1 Superoxide dismutase knockout (Sod−/−) mice*

There are two isoforms of SOD, the primary antioxidant enzyme in the retina that catalyzes the breakdown of potentially harmful ROS [28]. After 7 months of age, knockout mice lacking SOD1 (*Sod1*−/−) develop sub-RPE deposits that share similar composition to drusen found in human AMD. Other pathology in these mice include thickened BrM, RPE atrophy, and CNV in about 10% of mice [17]. This model, however, is also a model of amyotrophic lateral sclerosis resulting in extra-retinal phenotypes which can complicate the use of this mouse strain [29]. Similarly, mouse models transduced with an adenovirus-mediated ribozyme delivery system to inactivate SOD2 showed signs of oxidative damage like *Sod1*−/− models, with the caveat that SOD2 null mice did not show signs of CNV. Therefore, SOD2 depletion is not a good model for exudative AMD but may be useful for studying non-exudative AMD [17, 28].
