*2.3.4 Cluster of differentiation 46 (Cd46−/−) mice*

Like CFH regulating C3b, CD46 is a regulatory cofactor that aids in inactivating C3b and C4b. *Cd46*−/− mice at 12 months of age exhibit increased complement in the RPE with hypertrophic and vacuolated RPE. These findings along with increased autofluorescence, lipofuscin, and autophagosomes of the RPE suggest degeneration of this retinal layer. Other findings in these mice include sub-RPE deposits with thickening of BrM, decreased choriocapillary lumen and fenestrations, and decreased number of nuclei in the outer nuclear layer of the retina. In this model there were low levels of VEGF and no signs of neovascularization, positioning this mouse as a model to the study of non-exudative AMD [26].

#### *2.3.5 Inflammasome mice*

Inflammasomes are multiprotein complexes that respond to pathogen-associated molecular patterns or other cellular stresses. Inflammasome activation leads to secretion of proinflammatory substances such as caspase-1, interleukin-1β (IL-1β), and interleukin-18 (IL-18). The NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been implicated in many inflammatory conditions such as gout, autoimmune diseases, atherosclerosis, and AMD [32]. Eyes with GA have lower levels of Double-Stranded RNA-Specific Endoribonuclease (DICER1), a micro-RNA, which leads to increased levels of Arthrobacter luteus (Alu) RNA. Alu RNA activates the NLRP3 inflammasome leading to increased levels of myeloid differentiation primary response 88 (MYD88) and IL-18 and ultimately causing RPE atrophy [26]. However, in *Myd88*−/− mice and *Il18r1*−/− mice, Alu RNA did not cause RPE degeneration [33]. These findings suggest that inflammasome activation may have a role in AMD pathogenesis and present potential targets for future therapies.

*An Overview of Age-Related Macular Degeneration: Clinical, Pre-Clinical Animal Models… DOI: http://dx.doi.org/10.5772/intechopen.96601*
