I am an assistant professor (tenure track) in the department of neuroscience at the University of Toledo. Building upon my expertise, both in experimental and computational aspects of neuroscience, I seek to determine the similarities and diversities associated with psychiatric disorders and develop a "grand unified theory" explaining these disorders. My thinking on this long-envisioned project originated during my Ph.D. studies at the National Institute for Basic Biology, Okazaki, Japan. Here, I was trained in various aspects of molecular biology and histology, and my dissertation involved exploring the comparative anatomy of the serotonergic system in human, macaque, and marmoset brains. Intrigued about the role of serotonin and other monoaminergic systems in psychiatry, I shifted from basic science to psychiatric research for my postdoctoral studies at the University of Toronto. Here, I worked with an age-by-disease interaction model that employs the principle of using aging as a reference to understand the baseline homoeostatic changes and then compares psychiatric disorders as deviations from the baseline. To further develop this model, I spearheaded two subsequent projects. In the first, I studied age-associated transcriptomic changes at the cellular and bulk tissue levels. This study provided a reference to evaluate molecular homeostasis associated with transcriptomic changes in Major Depressive Disorder (MDD). While handling these projects, I established a robust single cell-type collection and RNA sequencing technique and developed a bioinformatics analysis pipeline not only for interpreting the resulting data but also for segregating causal and consequential pathways leading to MDD. As a faculty, I have broadened the scope of my research program, and my current initiatives include: First, expand the age-by-disease interaction model to explore the age-altered kinome-transcriptome correlation at the cellular level. Second, developing a pipeline to integrate single-cell transcriptomics with biophysical microcircuitry modeling and developing cell-specific therapeutics using (potential) causal inference. Considering its penetrant nature, I am using epilepsy as a model to develop this pipeline and propose testing therapeutic or disease-modifying drugs using electroencephalogram (EEG) recordings in a mouse model of epilepsy. Demonstrating my originality and productivity, this year (2021-22) I published five senior/communicating author articles centered on my research program, totaling 47.05 impact factors, and have deposited several others on preprint servers.