Kevin Noguchi

Kevin Noguchi

Associate Professor of Psychiatry

Additional Titles & Roles

  • Intellectual And Developmental Disabilities Research Center Core Faculty
  • Co-Leader Neuropathology Unit – Model Systems Core

Education & Training

  • PhD: Behavioral Neuroscience: University of California, Los Angeles, CA, 2003
  • CPhil: Behavioral Neuroscience: University of California, Los Angeles, CA, 2001
  • MA: Behavioral Neuroscience: University of California, Los Angeles, CA, 1998

Major Awards

  • K01 NIMH Mentored Research Scientist Career Development Award, 2009

Research Interests

My research focuses on drug-induced neuropathology in the developing 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. Using animal models, we have found GABA agonists and NMDA antagonists are relatively safe in the adult but can be highly toxic to the developing brain. These two classes of drugs include all general anesthetics, sedatives, anti-epileptics drugs, and many drugs of abuse (such as alcohol, ketamine, phencyclidine, and ketamine). Clinically, this suggests anesthesia/sedation may have adverse effects for over a million children that are exposed to anesthesia every year. This concept has recently been bolstered by several retrospective clinical studies showing children exposed to anesthesia exhibit neurodevelopmental impairment. However, it is important to acknowledge that anesthesia is oftentimes an important and necessary component of perinatal medicine. Therefore, we are characterizing when the developing brain is susceptible to this toxicity and working on safer ways to administer anesthesia. We also study the adverse effects glucocorticoids can have on the developing brain. Approximately 10% of prematurely born infants receive glucocorticoid therapy to treat respiratory dysfunction associated with premature birth. However, clinical exposure to these drugs can cause permanent neuromotor/cognitive deficits and selective cerebellar stunting. Using animal models, I have found exposure to glucocorticoids produces rapid apoptosis in the neural progenitor cells of cerebellar external granule layer and permanent stunting of the cerebellum. Like anesthesia, glucocorticoids are oftentimes an important part of appropriate perinatal care. Therefore, we are also working on safer ways to administer this therapy.

Beyond drug-induced neuropathology, we also study the neurotoxic effects of Zika virus infection on the fetus. Since the discovery of its spread to Brazil in April 2015, the Zika virus has gone from a little known pathogen to a global health emergency of international concern (World Health Organization designation). It was estimated that 1.3 million Brazilians were infected by the end of 2015 which is projected increase to 4 million in the Americas by the end of 2016. Of even greater concern, the Center for Disease Control has concluded that there is a causal relationship between Zika infection and fetal abnormalities which include microcephaly (abnormally small head), intrauterine growth restriction, and fetal demise. Virtually nothing is known about the neuropathologic sequelae of Zika infection despite these devastating effects. Therefore, we have recently begun collaboration with the Diamond and Miner labs to explore how this occurs in their mouse models of Zika infection.

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Key Publications

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    Funded Research Projects

    R01 NICHD (PI): Anesthesia toxicity in neonatal primate brain

    R01 NICHD Administrative Supplement (PI): Anesthesia toxicity in neonatal primate brain

    R01 NICHD (Key Personnel): Hypothermia to prevent neurotoxic side effects of pediatric drugs

    U54 NICHD (Neuropathology Unit: Core Faculty): Washington University Intellectual And Developmental Disabilities Research Center