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Edward Brodkin, MD

Brodkin Lab, Social Neuroscience Laboratory

125 S. 31st Street
Room 2220
Philadelphia, PA 19104

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I am a psychiatrist with an interest in the biological basis of social behavior disruptions in autism spectrum disorders (ASD) and other neurodevelopmental disorders. My laboratory research is focused on the neurobiology of sociability (tendency to seek social interaction) and aggressive behaviors. The biological basis of social behavior disruptions in ASD is only beginning to be made clear, and currently available treatments are inadequate for addressing these social disabilities. Learning more about the fundamental biology of social behaviors can ultimately lead to the development of novel and more effective treatments for individuals with ASD.

My laboratory group uses the mouse as a model organism for biological studies of social behaviors. These studies may have relevance to human brain and behavior. For virtually every mouse gene, there is a homologous human gene, and vice versa. Animal studies may help to clarify the function of candidate genes and neurobiological pathways that may be involved in ASD and other human neurodevelopmental disorders.

Our studies indicate that the BALB/cJ inbred mouse strain shows reduced sociability and other behavioral and neurobiological traits relevant to ASD (Sankoorikal et al., 2006; Brodkin, 2007). A new set of studies in our laboratory is aimed at testing the developmental relationships among brain growth, brain white matter abnormalities, and sociability in the BALB/cJ strain. In another project, we have used a whole genome scan to identify genomic loci on chromosome 10 and chromosome X that affect intermale aggressive behaviors in mice (Brodkin et al., 2002), and we are currently testing the role of specific candidate genes and neurobiological pathways in these behaviors.

I collaborate with other members of the Center for Autism Research to develop translational studies of social behaviors in ASD that can help uncover the fundamental neurobiological mechanisms and thus can lead to development of novel treatment approaches. Future collaborative projects will include parallel human and mouse model studies of autism candidate genes, brain growth and development, and social behavior development.

Clinically, I have an interest in using knowledge gained from basic neurobiological and genetic studies to improve treatment for individuals with ASD. I also focus on transition-to-adulthood issues for individuals on the spectrum and on helping these individuals obtain and retain employment.

Sample of Significant Publications

Brodkin ES. BALB/c mice: low sociability and other phenotypes that may be relevant to autism. Behavioural Brain Research (Special Issue: “Animal Models for Autism”). 2007. 176: 53-65.

Brodkin ES, Goforth SA, Keene AH, Fossella JA, Silver LM. Identification of quantitative trait loci that affect aggressive behavior in mice. Journal of Neuroscience. 2002. 22: 1165-1170.

Chevallier, C., Kohls, G., Troiani, V., Brodkin, E.S., Schultz, R.T. (in press). The Social Motivation Theory of Autism. Trends in Cognitive Sciences.

Sankoorikal GMV, Kaercher KA, Boon CJ, Lee JK, Brodkin ES. A mouse model system for genetic analysis of sociability: C57BL/6J vs. BALB/cJ inbred mouse strains. Biological Psychiatry. 2006. 59: 415-423.

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