Yoshimizu T, Pan JQ, Mungenast AE, et al. Functional implications of a psychiatric risk variant within CACNA1C in induced human neurons. Mol Psychiatry. 2015;20(2):162–169.
Bavamian S, Mellios N, Lalonde J, et al. Noncoding RNAs connect genetic risk factors to the neurodevelopmental basis of bipolar disorder. Mol Psychiatry. 2015;20(5):548.
Madison JM, Zhou F, Nigam A, et al. Characterization of bipolar disorder patient-specific induced pluripotent stem cells from a family reveals neurodevelopmental and mRNA expression abnormalities. Mol Psychiatry. 2015;20(6):703-17.
Jon Madison, Ph.D.
Jon Madison is a group leader and research scientist II for the Translation and Therapeutics Group of the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard, working under the direction of Jeff Cottrell. Madison studies the functions of genes and proteins associated with schizophrenia, autism, and bipolar disorder using both functional genomic approaches and small molecules. By understanding the biochemical pathways that confer risk for psychiatric disease, the group hopes to develop more effective therapeutics. His group currently studies a subset of genes and protein complexes associated with autism and schizophrenia that are part of the ubiquitin proteasome pathway.
Before joining the Broad Institute in 2007, Madison earned his bachelor’s degree in chemistry at Duke University and obtained his Ph.D. in genetics at Harvard University. His postdoctoral research in neurobiology was undertaken at Tufts Medical School, the University of California, Berkeley, and Massachusetts General Hospital. He is a recipient of The Brain and Behavior Research Foundation (formerly NARSAD, the National Alliance for Research on Schizophrenia and Depression) 2010 Young Investigator Award.
Contact Jon Madison via email at firstname.lastname@example.org.