Edward S. Brodkin, M.D.|
Assistant Professor of Psychiatry
Center for Neurobiology and Behavior
Perelman School of Medicine
Translational Research Laboratory, Room 2220
125 S. 31st Street
Philadelphia, PA 19104-3403
EDUCATION: B.A. 1988, Harvard University (History of Science)
B.A. 1988, Harvard University (History of Science)
Our laboratory uses methods of genetics and genomics to dissect the neurobiological pathways mediating social behaviors, including aggression and sociability (tendency to seek social interaction). Certain neuropsychiatric disorders, including autism and schizophrenia, are characterized by extremely disabling disturbances in social cognition and socioemotional behaviors. Currently available treatments are inadequate for ameliorating these social disabilities. Elucidating the fundamental biology of affiliative and aggressive behaviors may ultimately lead to the development of novel treatments for autism and other major neuropsychiatric disorders. Our laboratory is focused on the following major questions of interest:
Currently, most of our genetic studies of social behaviors use the mouse as a model organism, because of the experimental control that a model organism provides, and because of the many resources available for mouse genetics. These studies may have relevance to human brain and behavior. For virtually every mouse gene, there is a homologous human gene, and vice versa. Moreover, the genetic and neurobiological pathways underlying primitive social behaviors, such as aggression, appear to have been conserved, to some extent, across mammalian evolution. Thus, animal studies may help to identify candidate genes and neurobiological pathways that may be involved autism or other human neuropsychiatric disorders. Previously, in a whole genome scan, we identified quantitative trait loci (QTLs) on chromosome 10 and chromosome X that affect intermale aggressive behaviors in a cross of NZB/B1NJ and A/J inbred mice (Brodkin et al., 2002). Currently, we are fine-mapping these genetic loci by breeding interval-specific congenic strains, and we are sequencing and analyzing positional candidate genes for aggression. We also are using single-gene mutant mice (e.g. knockouts) to dissect pathways that mediate aggressive behaviors.
In addition to our work on aggressive behaviors, we have demonstrated differences among inbred mouse strains in sociability, using a social choice behavioral paradigm (Brodkin et al., 2004; Sankoorikal et al 2006). Our studies indicate that the BALB/cJ inbred strain shows reduced sociability and other behavioral and neurobiological traits relevant to autism (Brodkin, in press). A new set of studies in our laboratory is aimed at elucidating the brain pathways that underlie this reduced sociability of BALB/cJ mice. Also, we have initiated studies of mice with knockouts of autism candidate genes. We are also involved in human psychiatric genetic studies in collaboration with other investigators at University of Pennsylvania (see, for example, ccn.upenn.edu and ccn.upenn.edu/home/people/affiliates.shtml).
Dr. Brodkin is also a co-founder and attending psychiatrist in the Penn Adult Social Learning Disorders program for patients with Asperger syndrome, high-functioning autism, schizoid or avoidant personality, social phobia, and related conditions (see www.med.upenn.edu/add/brodkin.shtml and www.med.upenn.edu/add/treatment_sld.shtml). This program is dedicated to clinical care for patients, as well as translational research relevant to human social behaviors and social cognition. Our hope is that this research will ultimately improve the clinical care of individuals with these disorders.
Work in the Brodkin lab has been funded by various agencies, including the National Institute of Mental Health, the Cure Autism Now Foundation, the Burroughs Wellcome Fund (Career Award in the Biomedical Sciences, E.S. Brodkin recipient), the University of Pennsylvania University Research Foundation, the National Alliance for Research on Schizophrenia and Depression (NARSAD), the Mental Retardation and Developmental Disabilities Research Center of the Children’s Hospital of Philadelphia, the Philadelphia Foundation, and the University of Pennsylvania McCabe Fund.