Age-related macular degeneration (AMD) is the leading form of vision loss in humans 40 years and older. Mutations in the gene encoding the innate immune regulatory protein, complement factor H (CFH), have been implicated in AMD but do not explain all instances. CFH functions to protect host cells from unwanted immune activation by sensing a surface-bound biomolecule called sialic acid. Sialic acids are species specific and, in conjunction with other molecules, form our individual molecular identities. In humans, a major alteration in the make-up of our sialic acid composition, compared to the great apes, resulted in a molecular watershed with numerous evolutionarily significant ramifications. Unlike our closest living relatives, humans also have a remarkably long post-reproductive life-span, which is theorized to maximize survival of young relatives through caregiving and knowledge transmission by grandparents. As a consequence of our long lives, numerous post-reproductive diseases, such as AMD, affect the elderly population. To explore other causal mechanisms of AMD, this thesis proposes a potential involvement of altered sialic acids in eye tissue compromising CFH function in absence of AMD-causing CFH mutations. The combined findings from preliminary experiments confirm the abundance and distribution of sialic acid in retinal tissue. The correlation between total sialic acid content and CFH appears to support the hypothesis of a link between retinal sialome CFH function. However, the lack of difference between healthy and AMD samples do not support a direct involvement of a compromised sialome in the pathology of AMD.