Originally from Salt Lake City, Utah, Ben holds a biology degree from the University of Utah. Ben then completed his graduate studies working with Dr. Brian Popko at The University of Chicago. As a graduate students Ben’s research focused on exploring the role of the integrated stress response in hypoxic injury to glial cells. Ben then moved to Case to train as a postdoctoral fellow with Dr. Paul Tesar where he established a phenotypic screening platform for identifying small-molecule suppressors of pathological reactive astrocyte states. As postdoc Ben was awarded a Career Transition Award from The National Multiple Sclerosis Society to further study the intrinsic and extrinsic mechanisms of glia cell pathology in MS. Ben joined the Department of Genetics and Genomes Sciences at ÐÇ¿Õ´«Ã½ as an Assistant Professor in June 2024 and is a member of the Institute for Glial Sciences
Research Information
Research Projects
The goal of my research program is to define the molecular mechanisms that regulate how glial cells take on harmful or beneficial cell states in health and disease.
I am particularly interested in how astrocytes, the most abundant glial cell in the brain, become reactive in response to different stimuli, and how these reactive astrocytes enhance or impede oligodendrocyte formation in development and disease. To accomplish this, my lab develops advanced cellular platforms for studying astrocytes and astrocyte-oligodendrocyte interactions at scale. We then leverage these platforms for genetic and chemical screening to identify putative regulators of astrocyte reactivity for deeper mechanistic interrogation. Finally, the in vivo relevance of these regulators and their potential as reactive astrocyte targeted therapeutics is determined using mouse genetics and mouse models of disease.
Ultimately, my lab will advance our understanding of glial biology in order to develop novel glial targeted therapeutics for the treatment of neurological diseases.