Current Research and Scholarly Interests
I am an Assistant Professor in Psychiatry and Behavioral Sciences at Stanford University School of Medicine starting in January 2020. A long-term goal of my lab is to understand how glial cells sculpt neural circuits, focusing on the molecular modulators allowing glia their dynamic nature. I have a decades-long history of identifying difficult problems and applying novel approaches for investigation. This has resulted in numerous examples of scientific accomplishments, including discovering that circadian dysregulation decreases neural precursor cell proliferation and differentiation and consequent cognitive function (Gibson et al., 2010, PLoS ONE), demonstrating that neuronal activity modulates myelination in vivo (Gibson et al., 2014, Science), discerning the signaling mechanisms mediating myelin plasticity in health and aplasticity in disease (Geraghty, Gibson et al., 2019, Neuron), identifying tri-glial dysregulation driven by activated microglia as a fundamental cellular disruption associated with the neurological disorder following chemotherapy treatment (Gibson et al., 2019, Cell), and identifying the molecular circadian clock as a key molecular regulator of myelin-forming glia which in turn modulates sleep architecture (Rojo et al., 2023, Neuron). My lab is also very interested in the mechanisms mediating human myelination as the majority of our knowledge is derived from imaging studies. To assess the functional myelin capacity of human oligodendrocytes, we developed an ex vivo myelin platform using organotypic brain slice cultures derived from shiverer mice that lack compact myelin in which we can seed human iPSC-derived oligodendrocytes that are then able to myelinate the axons of the shiverer slice (Tsarouchas et al. 2025). This platform allows for precise evaluation of human oligodendrocyte myelin capacity in a pseudo-intact microenvironment. My integrated research background studying myelin biology affords me a unique position to study the cell intrinsic and microenvironmental mechanisms of glial cell population dynamics in both normal development, aging, and disease models, specifically related to brain disorders that include myelin abnormalities like autism spectrum disorders, multiple sclerosis, and Alzheimer’s disease. We use both mouse modeling and patient-derived iPSCs to study oligodendroglial maintenance and maturation during development and dys/demyelinating diseases.
