Dr. Levitt received his BA in Biological Sciences from the University of Chicago, PhD in Neuroscience at the University of California, San Diego. He completed a postdoctoral fellowship in Neuroscience at Yale University. Dr. Levitt has held leadership positions at University of Pittsburgh, Vanderbilt University and University of Southern California.
Dr. Levitt was elected as a member into the prestigious Institute of Medicine (IOM), part of the National Academy of Sciences. Named a McKnight Foundation Scholar in 2002, Dr. Levitt also was a MERIT awardee from the National Institute of Mental Health and served as a member of the National Advisory Mental Health Council for the National Institute of Mental Health. He is an elected Fellow of the American Association for the Advancement of Science (AAAS), Chair-elect of the Neuroscience Division of the AAAS, and an elected member of the Dana Alliance for Brain Initiatives.
He is a Senior Fellow at the Center for the Developing Child at Harvard University, and serves as Scientific Director of the National Scientific Council on the Developing Child, a policy council that brings the best research from child development and neuroscience to assist policy makers and business leaders in making wise program investment decisions.
He is a member of a number of scientific advisory boards for foundations and university programs, served as Senior Editor for Journal of Neuroscience, and currently serves on the editorial boards of eLife, Neuron, Cerebral Cortex, Autism Research, Journal of Neurodevelopmental Disorders and Disease Models and Mechanisms. Dr. Levitt’s research focuses on the development of brain architecture that controls learning, emotional and social behavior.
His research focuses on genetic and environment factors that increase risk for neurodevelopmental and neuropsychiatric disorders, such as autism and schizophrenia. His clinical research studies address autism heterogeneity by studying children with autism who also have co-occurring medical conditions, such as gastrointestinal disorders, with the goal of developing better diagnostic criteria and personalized treatments.
He has published over 250 papers.
BA, Biological Sciences, University of Chicago; PhD, Neurobiology, University of California, San Diego
National Institutes of Health, NIMH R01 MH067842, July 2002 - June 2013, Function and Structure Adaptations in Forebrain Development; National Institutes of Health, NIDA R01 DA022785, September 2007 – July 2012, Development of Reciprocal Neural Circuitry; National Institutes of Health, NIMH R01 MH080759, September 2007 – August 2012, Neurodevelopmental Mechanisms of Social Behavior; National Institutes of Health, NIMH Conte Center P50 MH078028 (Project 2) September 2007 – June 2012, Serotonin as a Modulator of Axon Guidance Signals; Simons Foundation Autism Research Initiative Behavioral and Physiological Consequences of Disrupted Met Signaling, July 2009 – June, 2012
Wu, H., Levitt, P. Prenatal expression of MET receptor tyrosine kinase in the fetal mouse dorsal raphe nuclei and visceral motor/sensory brainstem. Develop. Neurosci. 35:1-16 2013.
Eagleson, K.L., Milner, T.A., Xie, Z., Levitt, P. Synaptic and extrasynaptic location of the receptor tyrosine kinase Met during postnatal development in the mouse neocortex and hippocampus. J. Comp. Neurol. 521:3241-3259, 2013.
Aldinger, K.A., Plummer, J.T. and Levitt, P. Comparative DNA methylation among females with neurodevelopmental disorders and seizures identifies TAC1 as a MeCP2 target gene. J. Neurodevelop. Disorders, 5:15, 2013.
Gorrindo, P., Lane, C.J., Lee, E.B., McLaughlin, B.A., Levitt, P. Enrichment Of Elevated Plasma f2t-Isoprostane Levels In Individuals With Autism Who Are Stratified By Presence of Gastrointestinal Dysfunction. PLoS One 8:e68444, 2013.
Plummer, J.T., Evgrafov, O.V., Bergman, M.Y., Friez, M., Haiman, C.A., Levitt, P., Aldinger, K.A. Transcriptional regulation of the MET receptor tyrosine kinase gene by MeCP2 and sex-specific expression in autism and Rett syndrome. Transl. Psychiatry 3:e316, 2013.
Gorrindo, P., Williams, K.C., Lee, E.B., Walker, L.S., McGrew, S.G., Levitt, P. Gastrointestinal dysfunction in autism: parental report, clinical evaluation and associated factors. Aut. Res. 5:101-108, 2012.
Qiu, S., Aldinger, K.A., Levitt, P. (2012). Modeling of Autism Genetic Variations in Mice. Focusing on Synaptic and Microcircuit Dysfunction. Dev. Neurosci. 34:88-100.
Reeb-Sutherland, B.C, Levitt, P., Fox, N.A. The predictive nature of individual differeneces in early associative learning and emerging social behavior. PLoS One 7:e30511, 2012.
Rudie, J.D., L. M. Hernandez, L.M., Brown, J.A., Beck-Pancer, D., N. L. Colich, N.L., Gorrindo, Thompson, P.M., Geschwind, D.H., Bookheimer, S.Y., Levitt, P., Dapretto, M. Autism Associated Promoter Variant in MET Impacts Functional and Structural Brain Networks. Neuron, 75:904-915, 2012.
Reeb-Sutherland, B.C., Fifer, W.P., Byrd, D.L., Hammock, E.A.D., Levitt, P., Fox, N.A. One month old human infants learn about the social world while they sleep. Develop. Sci., 2011, 14:1134-1141, 2011.
Genetic and environmental factors that cause autism spectrum disorders (ASD)
Clinical studies of children with ASD who also have co-occurring medical symptoms
Development of neural circuitry that controls social-emotional behavior and learning
Role of the placenta in influencing fetal brain development and long-term healthy outcomes
The projects in our laboratory are driven by a talented group of research fellows, graduate students, research staff and collaborating faculty. We focus on investigating the development of brain architecture that controls learning, emotional and social behavior.
Our research studies have a long-term goal of understanding the biological basis of neurodevelopmental and neuropsychiatric disorders, and how genes and the environment (prenatal or early postnatal) together influence typical and atypical development. We use preclinical models, gene manipulations, and exposure to early adverse stressful experiences to study the impact on circuit wiring and the development of social and emotional behaviors. We study the interaction between developmental learning mechanisms and social behavior in human infants and model systems. We study how the expression of genes are controlled, particularly genes that influence circuit wiring, and how growth factor receptors that are risk factors for autism work to control synapse maturation.
Using genetics, measurement of biomarkers and deep clinical characterization, we study children with autism spectrum disorder, and those subgroups that have prevalent co-occurring medical conditions, such as gastrointestinal disorders. In experimental model systems, we connect autism risk genes and medical conditions by manipulating expression of relevant genes in the gut. Studies also focus on genetic manipulation of genes expressed in the in vivo placenta that regulate production of the neurotransmitter serotonin. We seek to understand how disruption of these genes in the placenta influence fetal brain development and long-term behavior. An array of technical methods are used, including conditional gene targeting, biochemistry and molecular biology, microscopy, cell culture and in utero electroporation, neuroimaging, electrophysiology and behavioral analyses.
In The News- Press Releases
- Researchers Unravel Role of Oxidative Stress in Autism Spectrum Disorder
- Children’s Hospital Los Angeles Names Inaugural Director of Developmental Neurogenetics Program Within the Institute for the Developing Mind
- National Institutes of Health (NIH)
- Simons Foundation