Age-related macular degeneration (AMD) is the leading cause of blindness in Scotland. While the early stages of AMD do not influence visual acuity and are mainly characterized by yellowish deposits called drusen, late stage AMD can cause severe vision impairment and eventually leads to incurable blindness. Despite recent advances in treatment of the neovascular form of AMD, the underlying cause of vision loss is the death of photoreceptors which cannot currently be slowed or halted. Since the prevalence of AMD steadily increases with age, it will continue to be a major individual and societal burden in our aging population. With advanced age, our cells lose the ability to maintain the stability and integrity of our genetic material. Often, whole chromosomes are lost or multiplied and affected cells are expected to behave differently than normal cells. Crucially, my group recently showed that changes in Y chromosome abundance in blood is a strong risk factor for AMD.
Building on those results, we now want to investigate how genomic DNA abundance of other chromosomes can influence the risk to develop either the early stages of AMD or the sight-threatening late stage forms. Using modern, high-throughput molecular methods allows us to further understand how chromosomal abundance is influencing the function of genes and gene networks in cells. The aim is to identify the key mechanisms affected by chromosomal abundance and to understand how those shape the risk and outcome of AMD. Understanding those processes is crucial to identify new targets for AMD treatment.
Taken together, the proposed analyses will not only shed light onto the role of chromosomal abundance in AMD, but also shed light on the molecular basis of aging. Our work has the potential to improve AMD risk prediction and may be useful for the development of novel and tailored AMD therapies.
APPLICATION PROCEDURE:
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