My long-term goal is to contribute to our understanding of the cellular and molecular pathogenesis of retinal degenerative diseases. A complete list of my publications is available here.
The diversity of blinding diseases makes it challenging to develop therapies to prevent vision loss. However, despite their differences, retinal degenerations typically end in photoreceptor death, suggesting they may share common pathogenic mechanisms. The first major aim of my dissertation research focused on the role of metabolic dysfunction in photoreceptor death. Our studies indicate that NAMPT-mediated NAD+ biosynthesis is essential for photoreceptor survival and function and that retinal NAD+ deficiency is a common feature of blinding diseases. My findings offer novel therapeutic strategies for facilitating photoreceptor survival in retinal degenerative diseases independent of their underlying etiology. We published our findings in Cell Reports (press release here).
The second major aim of my dissertation research focused on age-related macular degeneration (AMD), a major cause of vision loss in older adults. Past studies in the Apte lab have established that immune cells called macrophages undergo functional changes as they age and that these age-associated changes promote diseases of the elderly, including AMD. However, the molecular and cellular pathways that regulate macrophage aging were unclear. My research demonstrated that microRNA-150 plays a pivotal role in skewing macrophages towards the aged phenotype by regulating lipid homeostasis in macrophages. We published our findings in JCI Insight (press release here).