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Zoology and Physiology
Office: Biological Sciences room 314F
About me: I earned my PhD in Biology from the National Institute for Basic Biology, Japan, where my dissertation explored the anatomy of serotonergic infrastructure, including receptors and transporters, across human, macaque, marmoset, and mouse brains. Intrigued about the role of serotonin and other monoaminergic systems in psychiatry, I switched from basic science to translational psychiatric research for my postdoctoral studies at the University of Toronto. This transition expanded my research horizons into behavioral, experimental, and computational domains. My present work focuses on understanding the similarities and differences between psychiatric disorders and their cellular and molecular underpinnings. Something that has intrigued me recently are the ribosomes, and I am dwelling on my hypothesis that these tiny molecular machines, with their mobility around neurons, are responsible for the variable presentation of mood (and other psychiatric) disorders.
Major Research Focus of NeuroPsych Group:
Ribosome Heterogeneity and Mood Disorders: Most stress paradigms downregulate RPGs and upregulate RP pseudogenes These dysregulations may cause stress-induced ribosomal specialization. Downregulated RPGs can change RP stoichiometry, while upregulated RPG pseudogenes can replace RPs with RP paralogs, creating a specialized ribosome. These hypotheses will be tested in postmortem major depression patients, chronic variable stress-exposed mice, and chronically glucocorticoid-stressed primary neurons.
Integrating single-cell transcriptomics and biophysical computer modeling to study stress and recovery: Using our novel single cell transcriptomics-based analytical pipeline, machine learning approaches, and parallels between the stress-related cell-types in the mouse and human, we will test the central hypotheses that the stress and stress recovery states are distinguished by distinct interactions between gut microbial and prefrontal cortex cellular profiles and that the non-pharmacological recovery state closely resembles the direct inverse. The findings will inform a biophysical model of the prefrontal cortex and predict novel therapeutics for reversing stress rather than compensating for it.