We identified three cmiRNAs which were significantly altered in NV AMD patients compared to AMD-free controls. Even when conditioned on covariates such as age, gender, smoking or Isoacteoside genetic risk scores computed from known AMD-associated variants, the three cmiRNAs showed little alteration in their association strength, indicating a true association with late stage NV AMD. In contrast, there was no association of cmiRNAs hsa-mir-301a-3p, hsa-mir361-5p, or hsa-mir-424-5p with GA AMD, suggesting subtypespecific cmiRNA profiles for late stage AMD. A global screening strategy similar to the one applied in this study may be suited to eventually characterize a GA AMD specific cmiRNA profile. Our initial discovery study comprised 9 NV AMD cases and 9 matched controls and identified several cmiRNA candidates with altered expression levels although none reached statistical significance after adjustment for multiple testing. A recent study compared cmiRNA levels in long-surviving versus short-surviving patients with lung cancer and found fold changes of significantly altered cmiRNAs between 1.60 and 7.15 and Cohen��s effect sizes between 0.92 and 1.54 which are considered to be large. Given the number of samples in our discovery study, we calculated the power to detect comparable effect sizes after adjustment for multiple testing. This would imply a power to identify between 4 and 33 cmiRNAs out of 100 in our discovery study at the assumed effect size or Cinnamyl-alcohol higher. To compensate for lower effect sizes, we increased our sample size to 276 individuals in the replication and retested individually the top 10 cmiRNAs hits from discovery. This uncovered a statistically significant association of NV AMD with cmiRNAs hsa-mir-301a-3p, hsa-mir-3615p, and hsa-mir-424-5p. Bioinformatical pathway analysis for genes suggested to be regulated by the NV AMD associated cmiRNAs were performed with two independent programs including the miRSystem and mirPATH v2.0. Both revealed concurring results and implicated the TGF-b and mTOR pathways in neovascular AMD pathology. Additionally, pathways closely related to the mTOR pathway were implicated by our analysis including WNT signaling, focal adhesion, neutrophin signaling and the insulin pathway.