
Additional Titles & Roles
- Executive Committee Member – Intellectual and Developmental Disabilities Research Center
Education & Training
- Ph.D.: University of California Los Angeles, 2003
- M.A.: University of California Los Angeles, 1998
- B.S.: University of California Santa Barbara, 1996
Major Awards
- K01 NIMH Mentored Research Scientist Career Development Award, 2009
Research Interests
My research primarily focuses on developmental neuropathology, including the effects of drugs and perinatal infection on the immature brain. Due to the intricate ontogenetic processes that occur during brain formation, drugs that are normally safe in the adult can be extremely toxic to the immature brain. We have found that acute exposure to drugs which are GABA agonists and/or NMDA antagonists can rapidly increase neurodegeneration in the developing brain. These two classes of drugs include general anesthetics, sedatives, anti-epileptics drugs, and drugs of abuse (such as alcohol, phencyclidine, and ketamine). This suggests several clinically administered drugs may be neurotoxic during the perinatal period despite being an important and necessary component of medical care. Our research is characterizing when the developing brain is susceptible to this toxicity and working on safer ways to administer them. We are also studying the safety of electronic cigarette (vaping) use during pregnancy which is being encouraged by numerous groups as a “harm reduction” strategy for pregnant smokers. While electronic cigarette use may produce less chemicals than traditional cigarettes, it also produces aerosols (which may contain GABA agonists or NMDA antagonists) we find neurotoxic to the developing brain.
Beyond drug-induced neuropathology, we also study the neurotoxic effects of viral infection on the fetus. Both the Zika and mpox viruses have gone from little known pathogens to global health emergencies of international concern (World Health Organization designation). If infection occurs during pregnancy, both viruses can vertically transmit to the fetus producing adverse effects ranging from microcephaly to fetal demise and miscarriage. Our goal is to study how these pathological effects occur and examine ways to mitigate their effects on the fetus.
Recent Publications
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The gain-of-function UBE3AQ588E variant causes Angelman-like neurodevelopmental phenotypes in mice
Weston, K. P., Gunelson, A. M., Maloney, S., Ge, X., Stelzer, J. A., Kim, K. S., Collier, S., Mindt, M. M., Agajanian, M. J., Major, M. B., Goldfarb, D., Noguchi, K. & Yi, J., Dec 2025, In: Scientific reports. 15, 1, 9152.
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MYT1L deficiency impairs excitatory neuron trajectory during cortical development
Yen, A., Sarafinovska, S., Chen, X., Skinner, D. D., Leti, F., Crosby, M. L., Hoisington-Lopez, J., Wu, Y., Chen, J., Li, Z. A., Noguchi, K. K., Mitra, R. D. & Dougherty, J. D., Dec 2024, In: Nature communications. 15, 1, 10308.
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Lacosamide and Levetiracetam Are Not Toxic to the Developing Mouse Brain
Noguchi, K. K., Palmer, C. W., Fuhler, N. A., Neblock, E., Fotedar, M. & Ikonomidou, C., Oct 2024, In: Annals of neurology. 96, 4, p. 812-818 7 p.
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Erratum: A MYT1L syndrome mouse model recapitulates patient phenotypes and reveals altered brain development due to disrupted neuronal maturation (Neuron (2021) 109(23) (3775–3792.e14), (S0896627321006814), (10.1016/j.neuron.2021.09.009))
Chen, J., Lambo, M. E., Ge, X., Dearborn, J. T., Liu, Y., McCullough, K. B., Swift, R. G., Tabachnick, D. R., Tian, L., Noguchi, K., Garbow, J. R., Constantino, J. N., Gabel, H. W., Hengen, K. B., Maloney, S. E. & Dougherty, J. D., Jul 3 2024, In: Neuron. 112, 13, p. 2257 1 p.
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Behavioral and Cognitive Outcomes of Rhesus Macaques Following Neonatal Exposure to Antiseizure Medications
Colman, R., Pierre, P., Adriansjach, J., Crosno, K., Noguchi, K. K. & Ikonomidou, C., Jan 2024, In: Annals of neurology. 95, 1, p. 57-70 14 p.