Abstract
Age-related macular degeneration (AMD) is a late-onset, neurodegenerative retinal disease that shares several clinical and pathological features with Alzheimer’s disease (AD) including extracellular deposits containing amyloid-β (Aβ) peptides. Immunotherapy targeting the Aβ protein has been investigated as a potential treatment for AD. Here, we present the rationale for extending this approach to treat AMD. We tested an anti-Aβ antibody administered systemically in a mouse model of AMD. Histological and functional measurements in treated animals compared to controls showed that following immunotherapy, the amounts of Aβ in the retina and brain were decreased and the ERG deficits in the retina were attenuated. These data support the hypothesis that Aβ is a therapeutic target for AMD.
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