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Kevin Noguchi, PhD

Current Position
Assistant Professor of Psychiatry

University Roles
Intellectual And Developmental Disabilities Research Center Core Faculty
Co-Leader Neuropathology Unit - Model Systems Core

Education and Training
B.S. Biopsychology, University of California, Santa Barbara
M.A. Behavioral Neuroscience, University of California, Los Angeles
C. Phil. Behavioral Neuroscience, University of California, Los Angeles
Ph.D. Behavioral Neuroscience, University of California, Los Angeles

Major Awards
K01 NIMH Mentored Research Scientist Career Development Award


Areas of 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. Much of this work is based on the pioneering work done by my mentor, Professor John Olney (recently deceased), who I have collaborated closely with and plan to continue his research. 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.


Key Publications
Noguchi KK, Johnson SA, Kristich LE, Martin LD, Dissen GA, Olsen EA, Olney JW, Brambrink AM (2016 Mar). Lithium Protects Against Anaesthesia Neurotoxicity In The Infant Primate Brain. Sci Rep. 6:22427.   Full Article ->

Miner JJ, Cao B, Govero J, Smith AM, Fernandez E, Cabrera OH, Garber C, Noll M, Klein RS, Noguchi KK, Mysorekar IU, Diamond MS, (2016 May). Zika Virus Infection during Pregnancy in Mice Causes Placental Damage and Fetal Demise. Cell. 165(5): 1081-1091.  Full Article ->

Noguchi KK, Walls KC, Wozniak DF, Olney JW, Roth KA, Farber NB (2008 Oct). Acute neonatal glucocorticoid exposure produces selective and rapid cerebellar neural progenitor cell apoptotic death. Cell Death Differ. 15(10): 1582-92.  Full Article ->

Noguchi KK, Cabrera OH, Swiney BS, Salinas-Contreras P, Smith JK, Farber NB (2015 Aug 25). Hedgehog regulates cerebellar progenitor cell and medulloblastoma apoptosis. Neurobiol Dis.   Full Article ->

Noguchi KK (2014 Jan 8). Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia. Cells. 3(1): 36-52.  Full Article ->

Noguchi KK, Lau K, Smith DJ, Swiney BS, Farber NB (2011 Aug). Glucocorticoid receptor stimulation and the regulation of neonatal cerebellar neural progenitor cell apoptosis. Neurobiol Dis. 43(2): 356-63.  Full Article ->


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

IDDRC Pilot Grant (PI): Zika induced neuropathology in the developing fetus