Marissa Scavuzzo is a postdoctoral fellow in Paul Tesar’s lab at Case Western Reserve University School of Medicine. She received her bachelor’s degrees in neuroscience and biology before earning her doctorate in developmental biology from Baylor University College of Medicine. In the Tesar Lab, she is studying the network of nervous system cells inside your gut that has been referred to as “the second brain.” Using lab-grown organs to mimic the human intestine, Scavuzzo is mapping the impact of support cells called enteric glia across a wide range of conditions including autism. In the brain, glia regulate and protect neurons in many different ways and contribute to neurodevelopmental and psychiatric diseases, but their role in the gut is a new field. Her goal is to understand how enteric glia shift states in autism and how these cells respond to genetic, environmental and dietary changes. For this work, she has been awarded the HHMI Hanna H. Gray Fellowship, the New York Stem Cell Foundation Druckenmiller Fellowship and the Hartwell Foundation Fellowship. She has also served as an invited speaker at national and international venues.
Principal Investigator: Paul Tesar
Undergraduate Fellow Project: Glial cell dysfunction in the “brain inside your gut”
Gut disturbances are unusually common in individuals with autism, however the basis of these gut defects are not yet known. As autism causes alterations to sociobehavioral function, much effort has been placed on understanding changes in the brain while intrinsic dysfunction of cells in people with autism in the gut remains unexplored. The enteric nervous system (ENS), colloquially known as the “second brain,” contains unique neuronal and glial cell types that collectively control gut function. We have generated three-dimensional intestinal “mini organs” innervated with the ENS from human induced pluripotent stem cells (iPSCs). In various conditions, including autism, glia in the brain can become reactive and polarize into a detrimental pro-inflammatory state that drives neuronal dysfunction and toxicity. Our preliminary data show that in autism, enteric glia upregulate key reactive markers compared to healthy controls. The presence of reactive enteric glia in autism has not previously been reported and their contribution to gastrointestinal dysfunction is unknown. In this project, our lab will use these innervated “mini-organs” to identify cellular and molecular changes in the enteric nervous system in autism and establish the prevalence of these defects across a panel of people with autism, both genetically defined and idiopathic.