I’m a neuroscientist researching the molecular and cellular mechanisms of perinatal brain development and how their maladaptation causes developmental brain disorders. Our lab is using rodent models to investigate neonatal hydrocephalus's genetic and cellular etiologies to find possible new therapeutic targets to improve neurocognitive outcomes.
Neonatal brains undergo layers of developmental changes and have very plastic potentials. I’m fascinated by the vigorously coordinated growth of young neural cells and how precisely they can communicate with each other among the same and between different cell types. One of our discoveries is that the loss of motile cilia gene in rodent brains reduces cerebrospinal fluid flow and neonatal hydrocephalus with delayed neural cell maturation and neuroinflammation. Our pre-clinical trials in these animals suggest that medical treatment to suppress neuroinflammation via microglia can improve brain function, neuronal maturation and myelination in neonatal hydrocephalus.
I feel fortunate to be able to study the amazing roles and communications of neonatal brain cells to discover new treatments for patients with developmental brain disorders. With recent advancements in tools and technologies in molecular neurobiology, we can view individual brain cells so closely that we can see how they react and communicate precisely. I hope to bring discoveries leading to better clinical management of neonatal brain disorders, including hydrocephalus.
I am honored to be a McLaurin Neurosurgery Scholar (2021). I also received a Pediatric Neurosurgery award from Cincinnati Children’s (2015), an Innovator Award from the Hydrocephalus Association (2017) and a Trustee Award & Procter Scholar (TAPS) from Cincinnati Children’s (2015). I’ve been a researcher for over 20 years, and I began my work at Cincinnati Children’s in 2013.
BS: Tokyo Gakugei University, 2000.
PhD: University of Tokyo, 2006.
Postdoctral training: University of Tokyo, 2007; Brigham and Women’s Hospital, Harvard Medical School, 2012.
Pediatric hydrocephalus; genetic basis of hydrocephalus; cellular basis of hydrocephalus; ependymal cell biology; choroid plexus and cerebrospinal fluid biology
Impaired neurogenesis alters brain biomechanics in a neuroprogenitor-based genetic subtype of congenital hydrocephalus. Nature Neuroscience. 2022; 25:458-473.
The Anti-Inflammatory Agent Bindarit Attenuates the Impairment of Neural Development through Suppression of Microglial Activation in a Neonatal Hydrocephalus Mouse Model. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2022; 42:1820-1844.
Neonatal hydrocephalus leads to white matter neuroinflammation and injury in the corpus callosum of Ccdc39 hydrocephalic mice. Journal of Neurosurgery: Pediatrics. 2020; 25:1-8.
Characterization of a novel rat model of X-linked hydrocephalus by CRISPR-mediated mutation in L1cam. Journal of Neurosurgery. 2020; 132:945-958.
Impaired neural differentiation and glymphatic CSF flow in the Ccdc39 rat model of neonatal hydrocephalus: genetic interaction with L1cam. DMM Disease Models and Mechanisms. 2019; 12:dmm040972.
A mutation in Ccdc39 causes neonatal hydrocephalus with abnormal motile cilia development in mice. Development (Cambridge). 2018; 145:dev154500.
Therapeutic value of prenatal rapamycin treatment in a mouse brain model of tuberous sclerosis complex. Human Molecular Genetics. 2011; 20:4597-4604.
Regulable neural progenitor-specific Tsc1 loss yields giant cells with organellar dysfunction in a model of tuberous sclerosis complex. Proceedings of the National Academy of Sciences of USA. 2011; 108:E1070-E1079.
Loss of Fyn tyrosine kinase on the C57BL/6 genetic background causes hydrocephalus with defects in oligodendrocyte development. Molecular and Cellular Neurosciences. 2008; 38:203-212.