The Hashimoto-Torii Lab

Alterations in the prenatal environment in utero affects fetal development. Harmful conditions, such as hypoxia, exposure to excessive levels of heavy metals, maternal smoking, and alcohol intake are thought to reprogram normal fetal brain development and consequently increase the incidence of many childhood disorders, including lower birth weight, SIDS, pediatric epilepsy, schizophrenia and ADHD.

However, molecular and cellular mechanisms underlying such reprogramming remain obscure. Dr. Hashimoto-Torii’s laboratory seeks to understand how adverse prenatal environments interact with genetic predisposition, thereby increasing disease susceptibility after birth. With a focus on maternal alcohol drinking, the team tackles this question through a combination of wet and dry experiments using mouse and human research models (supported by NIH/NIAAA). In addition, the lab is also testing potential drugs and devices to improve behavior problems of offspring after in utero exposure to harmful agents (supported by Scott-Gentle foundation).

 

The Torii Lab

Brain development consists of multiple dynamic processes ranging from cell type specification, proliferation, differentiation and migration, to neural circuit formation and refinement. Each of these processes has vulnerability to various genetic and environmental factors that cause structural and functional abnormalities in the brain.

The goal of our research is to decipher the complex mechanisms in which these factors impact normal brain development and to translate our findings into the development of novel therapeutic approaches for neurodevelopmental disorders such as schizophrenia and autism.

Our current interests include the mechanisms in which various neuronal subtypes are assembled into functional neural networks in the cerebral cortex, and how they go awry in neurodevelopmental disorders. Our lab uses combinations of cutting-edge tools and techniques, including in utero gene transfer, transgenic reporter mice, electrophysiology, proteomic and transcriptomic analyses, and encapsulation and transplantation of iPS cell-derived neural cells.

 

Variable expression of HSP70 in human neural progenitor cells exposed to oxidative stress