Anthony Sharkey Ricciardulli graduated from the University of California, Berkeley in 2017 with a B.S. in microbial biology. As an undergraduate, he investigated mechanisms of neurodevelopment during embryogenesis and developed expertise in cellular and molecular techniques. After graduation, he worked as a cellular engineer and tissue culture specialist in the laboratory of Fred Gage at the Salk Institute. There he generated patient-derived neurons to investigate how DNA repair processes and bioenergetics contribute to known neurodegenerative phenotypes using iPSC-derived human neurons. Prior to joining the Neuroscience Ph.D. Program at the University of Utah, he next worked at Sangamo Therapeutics, where his work focused on making AAV-delivered medicines targeting Parkinson’s disease, again using human iPSC-derived neurons to model this complex disease. Anthony joined the Neuroscience Ph.D. Program at the University of Utah where he has embarked on a joint project mentored by Nick Frost and Alex Shcheglovitov using three-dimensional human organoids to model circuit dysfunction in neurodevelopmental disorders.

Principal Investigator: Nicholas Frost

Fellow: Vy Nguyen
Undergraduate Fellow Project:

GRIN2b is a high-risk autism gene that encodes a glutamate channel subunit. Mutations in GRIN2b are linked to autism and result in pronounced cortical malformation including in cortical lamination deficits, more rapid brain development, disruption of gyri and macrocephaly. We are interested in understanding how these changes at the synaptic and cytoarchitectural level affect the representation of information relevant to behavior. To answer these questions, we will utilize three-dimensional organoids generated from human-derived iPSCs to understand cytoarchitectural and circuit level changes that result in abnormal microcircuit function during behavior. Fellows will have the opportunity to learn techniques ranging from cell culture and cellular differentiation to in vivo imaging of cellular activity during behavior, with the ultimate goal of understanding how mutations in GRIN2b influence the growth and complexity of cortical circuits, and how these changes at the cellular and circuit level affect computations performed by cortical networks.