**8. Genetics**

One prevailing approach in AMD research was the genome-wide association studies (GWAS) that have been used in attempt to predict risk of disease, understand pathogenesis, and identify potential therapeutic target [26]. GWAS have indeed identified several genetic loci, which harbor genetic variants known as single nucleotide polymorphisms (SNPs) that are associated with an increased risk of AMD. Factor H (CFH) represents the complement gene variant conferring the greatest quantitative statistical AMD risk. CFH inhibits a key activation step in complement activation, thereby reducing complement-induced host cell damage and inflammation [27]. The predictive power of AMD risk assessment can be

augmented greatly by considering genetic information from multiple loci in combination with epidemiologic and environmental risk factors. In contrast taking into consideration disease prevalence, the positive predictive value of genetic variation to assess AMD risk is inconclusive, even when multiple genetic loci are considered. Next-generation sequencing technologies combined with rigorous biological definition of mechanistic implications of the identified variants are likely to yield more valuable insights both into disease pathogenesis and rational development of novel diagnostics and therapeutics in the coming decade.
