Researcher | Research Overview
Glaucoma is one of the leading causes of blindness worldwide, and is thought to initiate with an insult to the axons of retinal ganglion cells (RGCs), which project their axons from the retina through the optic nerve to innervate targets in the brain. However, the precise mechanisms linking axonal injury to RGC apoptosis are unclear, and no therapies exist which can restore lost vision in patients. Recently, the Benowitz lab discovered that retinal interneurons play a critical role in linking optic nerve injury to RGC degeneration in mice.
Nicholas's long term research interests lie in understanding the molecular mechanisms underlying the interaction between injured neurons and their environment, with the aim of leveraging this understanding to facilitate neuronal regeneration in patients. Nicholas is currently studying the upstream signaling events linking optic nerve injury to RGC death, with the aim to identify clinically relevant interventions that lead to the preservation and regeneration of injured RGCs. This work was supported last year by the Molecular Bases of Eye Diseases Training Program at Schepens Eye Institute.
Researcher | Research Background
Nicholas received his B.S. in Biology with a double-major in Theatre from Boston College in 2010, and his PhD from the University of Texas at Austin in 2017. His dissertation research focused on the development and regeneration of the retinal pigment epithelium in zebrafish. This work resulted in multiple first-author publications as well as presentations in regional and international conferences, such as ARVO (2015, 2017), the Society for Developmental Biology (2016), and Society for Neuroscience (2018).
At Boston Children's Hospital, Nicholas is a Postdoctoral Research Fellow in the laboratory of Dr. Larry Benowitz. He leads a research project which involves multiple collaborations across institutions, mentors undergraduate research assistants, and is a board member of the BCH Postdoctoral Association in the Public Affairs Committee.