Dr. Levitt received his B.A. in Biology at the University of Chicago, a Ph.D. in Neuroscience at University of California, San Diego and a postdoctoral fellow at Yale University. Dr. Levitt has held chair and institute directorships at University of Pittsburgh Medical Center, Vanderbilt University and USC. Dr. Levitt has been a National Institute of Mental Health MERIT awardee, McKnight awardee, and has 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) and an elected member of the National Academy of Medicine.
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 state and federal policy makers and private sector business leaders in making decisions regarding child program investment.
His research program includes basic studies that probe the ways in which circuitries that controls learning, emotional and social behavior develop, using advanced technologies in genetics, cell biology and behavior. Clinical research investigates children with autism spectrum disorder who have co-occurring gastrointestinal and other conditions. Studies of infant resilience to adversity focus on the brain-based and metabolic changes that may have short and long-term impacts on mental and physical health. He has published over 275 scientific papers.
University of California, San Diego
Postdoctoral Fellow, Yale University School of Medicine
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
Bonnin, A., Goeden, N., Chen, K., Wilson, M.,L., King, J., Shih, J.C., Blakely, R.D., Deneris, E.S., Levitt, P. (2011) A transient placental source of serotonin for the fetal forebrain. Nature 472: 347-350.
Mukamel, Z., Konopka, G., Wexler, E., Osborn, G.E., Bergman, M.Y., Levitt, P., Geschwind, D.H. (2011) Regulation of MET by FOXP2, genes implicated in higher cognitive dysfunction and autism risk. J. Neurosci. 31:11437-11442.
State, M.W., Levitt, P. (2011) The conundrums of understanding genetic risks for autism spectrum disorders. Nat. Neurosci. 14:1-8.
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.
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. (2012) Autism Associated Promoter Variant in MET Impacts Functional and Structural Brain Networks. Neuron 75:904-915.
Gorrindo, P., Lane, C.J., Lee, E.B., McLaughlin, B.A., Levitt, P. (2013) Enrichment Of Elevated Plasma f2t-Isoprostane Levels In Individuals With Autism Who Are Stratified By Presence of Gastrointestinal Dysfunction. PLoS One 8:e68444.
Plummer, J.T., Evgrafov, O.V., Bergman, M.Y., Friez, M., Haiman, C.A., Levitt, P., Aldinger, K.A. (2013)Transcriptional regulation of the MET receptor tyrosine kinase gene by MeCP2 and sex-specific expression in autism and Rett syndrome. Transl. Psychiatry 3:e316.
Qiu, S. Lu, Z., Levitt, P. (2014) MET receptor tyrosine kinase controls dendritic complexity, spine morphogenesis and glutamatergic synapse formation in the hippocampus. J. Neurosci. 34:16166-16179, 2014.
Wang, F., Eagleson, K.L., Levitt, P. (2015) Positive regulation of neocortical synapse formation by Plexin-D1 receptor. Brain Research 1616:157-165.
Aldinger, K.A., Lane, C.J., Veenstra-VanderWeele, J., Levitt, P. (2015) Patterns of risk for multiple co-occurring medical conditions replicate across distinct cohorts of children with autism spectrum disorder. Autism Res., e-Ahead of Print.
Development of neural circuitry that controls social-emotional behavior and learning
Regulation of risk genes for neurodevelopmental disorders
Role of the placenta in influencing fetal brain development and long-term health outcomes
Clinical studies of children with ASD who also have co-occurring medical symptoms
Clinical neuroscience studies of resilience in very young children exposed to early adversity
The projects in our laboratory are driven by a talented group of postdoctoral fellows, graduate students, research staff and collaborating faculty. We focus on investigating the development of brain architecture that controls learning, emotional and social behavior, and the challenges that arise when development is derailed.
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 developing social behavior in model systems, and discover genetic and environmental influences on these complex behavioral relations. We study how the expression of genes is controlled, particularly genes that influence circuit wiring, synapse formation and maturation. An array of technical methods are used in our model system studies, including mapping of genes that regulate the developmental of complex behaviors, conditional gene disruption, biochemistry and molecular biology methods examining protein-DNA and protein-protein interactions, cell culture, and behavioral analyses.
Two clinical research programs are underway:
Tummy Troubles – The clinical study funded by Autism Speaks are measuring biomarkers, cognitive and social-emotional functions in school-age children with autism spectrum disorder who also have prevalent co-occurring medical conditions, particularly gastrointestinal disorders. Children are seen 3-4 times over a 1 year period to determine whether successful treatment of their GI conditions correlates with improved autism symptoms. In experimental model systems, we connect autism risk genes and medical conditions by disrupting expression of genes in brain and gut. For more information, contact Lisa Padilla at firstname.lastname@example.org
Infant resilience and early adversity – The clinical study is part of a large research consortium with Harvard’s Center for the Developing Child through a grant from The JPB Foundation in New York. Our studies include assessment of attention by modern eye tracking methods and simultaneous measures of brain wave activity (EEG). The study includes biomarker measures of oxidative stress in infants and their mothers who are screened for postpartum depression. For more information, contact Lisa Padilla at email@example.com
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