Treatments to enhance social functioning in adults with autism spectrum disorders. Neurobiology and genetics of of social behavior development, and neurobiology and genetics of autism and spectrum disorders.
autism; social; functioning; skills; behavior; motivation; emotion; genetics; genomics; neurobiology; brain
Measurement of social motivation, social approach, and social interactions in humans and animal models; behavioral genetics, genetic mapping, quantitative trait locus (QTL) analysis; neurobiological studies of social behavior phenotypes; psychosocial and biological treatments to improve social functioning.
Our laboratory is interested in the neurobiological and genetic mechanisms of social behavior development, as well as biological mechanisms underlying social motivation, social learning, and social skill acquisition and generalization. Certain highly heritable neuropsychiatric disorders, including autism and schizophrenia spectrum disorders, are characterized by reduced social motivation, increased social anxiety, disruptions in social learning, and impairment in social skill development. Despite its importance, the fundamental biology of these social processes is not well understood, and currently available treatments for these social behavior domains are inadequate.
Our current projects include the following: 1) Studies of treatments to enhance social motivation, social understanding, and social skills and reduce social anxiety in adults with autism spectrum disorder (ASD); 2) neural and genetic biomarkers in adults with ASD, 3) studies of the neurobiology and genetics of individual differences in social-emotional behavior development in humans and mouse models; 3) studies of gene-environment interactions in shaping social-emotional development.
Diagnosis and treatment of autism spectrum disorders in adults.
Fairless A.H., Shah R.Y., Guthrie A.J., Li H., Brodkin E.S.: Deconstructing sociability, an autism-relevant phenotype, in mouse models. The Anatomical Record (Special Issue: “New Concepts in Developing Brain Disorders--Autism”) 294: 1713-1725, 2011.
Dow H.C., Kreibich A.S., Kaercher K.A., Sankoorikal G.M.V., Pauley E.D., Lohoff F.W., Ferraro T.N., Li H., Brodkin E.S.: Genetic dissection of intermale aggressive behavior in BALB/cJ and A/J mice. Genes, Brain and Behavior 10: 57-68, 2011.
Fairless A.H., Dow H.C., Toledo M.M., Malkus K.A., Edelmann M., Li H., Talbot K., Arnold S.E., Abel T., Brodkin E.S.: Low sociability is associated with reduced size of the corpus callosum in the BALB/cJ inbred mouse strain. Brain Research 1230: 211-217, 2008.
Brodkin E.S.: Social behavior phenotypes in fragile X syndrome, autism, and the Fmr1 knockout mouse: Theoretical comment on McNaughton et al. (2008). Behavioral Neuroscience 122: 483-489, 2008.
Brodkin E.S.: BALB/cJ mice: low sociability and other phenotypes that may be relevant to autism. Behavioural Brain Research (Special Issue on “Animal Models for Autism”) 176: 53-65, 2007.
Sankoorikal G.M.V., Kaercher K.A., Boon C.J., Lee J.K., Brodkin E.S. : A mouse model system for genetic analysis of sociability: C57BL/6J vs. BALB/cJ inbred mouse strains. Biological Psychiatry 59: 415-423, 2006.
Gillihan S.J., Farah M.J., Sankoorikal G.M.V., Breland J., Brodkin E.S.: Association between serotonin transporter genotype and extraversion. Psychiatric Genetics 17: 351-354, 2007.
Brodkin E.S., Hagemann A., Nemetski S.M., Silver L.M. : Social approach-avoidance behavior of inbred mouse strains towards DBA/2 mice. Brain Research 1002: 151-157, 2004.
Brodkin E.S., Goforth S.A., Keene A.H., Fossella J.A., Silver L.M.: Identification of quantitative trait loci that affect aggressive behavior in mice. Journal of Neuroscience 22: 1165-1170, 2002.
Carlezon W.A., Thome J., Olson V.G., Lane-Ladd S.B., Brodkin E.S., Hiroi N., Duman R.S., Neve R.L., Nestler E.J.: Regulation of cocaine reward by CREB. Science 282: 2272-2275, 1998.
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Last updated: 03/22/2017
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