Age-related macular degeneration (AMD) is the leading cause of blindness in ageing societies and is caused by both environmental and genetic factors. The strongest genetic signal for AMD with odds ratios of up to 2.8 per adverse allele was found previously to center over two genes, ARMS2 and HTRA1 on 10q26, although with little knowledge as to the true functionally relevant gene or genetic variation. Due to extensive linkage disequilibrium (LD) at this locus, it was long assumed that the broad association signal cannot be dissected by statistical means. In this report, we have now separated the 10q26 region by analyzing imputed haplotypes with the help of a large case/control association data set. Rare recombinant haplotypes identified in 16,144 cases and 17,832 controls from the International AMD Genomics Consortium (IAMDGC), revealed genetic variants in ARMS2 but not HTRA1 to exclusively carry the AMD disease load with p values between 1.0x10(-773) and 6.7x10(-5) This study is a proof-of-concept and universally applicable to refine extended association signals providing the means to prioritize genes of interest for subsequent biological studies.