APOB and age-related macular degeneration: In AMD, the following evidence supports the “response to retention” hypothesis: (1) apoB100-containing lipoproteins accumulate in BrM in the same location as basal deposits and drusen, (2) oxidatively modified proteins and lipids are present in BrM; our laboratory has shown that oxidized apoB100 lipoproteins accumulate in BrM including drusen and basal deposits in AMD and that oxidized lipoproteins induce a pathologic phenotype to RPE cells [73], and (3) the accumulation of inflammatory mediators within drusen and basal deposits indicates a role for the innate immune response [50].