Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly, with no effective therapies for the dry form of the disease. Ding et al. extend studies that have implicated the deposition of amyloid β (Aβ) in AMD pathogenesis by demonstrating that systemic administration of a bispecific antibody targeting the two major forms of Aβ protects visual function and preserves the structure of the retinal pigmented epithelium in a mouse model that invokes factors that promote the onset of AMD. These dose-dependent effects were correlated with reductions in the levels of deposits containing Aβ and activated complement components, as well as increases in plasma Aβ concentrations. Immunotherapies targeting Aβ peptides have demonstrated that a reduction in amyloid plaques have improved cognitive function in mouse models of Alzheimer's disease. The identification of Aβ as a viable target for AMD therapy suggests that, regardless of their clinical value for treating Alzheimer's disease, Aβ-targeting antibody drugs and vaccines could be repurposed for preventing and/or treating AMD. (Proc. Natl. Acad. Sci. USA 108, E279–E287, 2011)