Academic Appointments


Administrative Appointments


  • Affiliate Scientist, California National Primate Research Center (2012 - Present)

Honors & Awards


  • George A. Miller Award, American Psychological Association
  • Kavli Fellow, U.S. National Academy of Sciences
  • Young Investigator Award, NARSAD
  • Distinguished Dissertation Award recipient, University of Michigan

Boards, Advisory Committees, Professional Organizations


  • Member of BRLE Grant Review Panel, National Institutes of Health (2012 - Present)
  • Editorial Board Member, Psychoneuroendocrinology (2013 - Present)
  • Associate Member, American College of Neuropsychopharmacology (2016 - Present)
  • Scientific Advisory Board Member, Stanford Autism Center at Packard Children’s Hospital (2016 - Present)

Professional Education


  • Postdoctoral, Stanford University, Psychiatry Neuroscience
  • Ph.D., University of Michigan, Biological Psychology
  • A.B., University of Michigan, Psychology

Current Research and Scholarly Interests


The core interest that guides the Parker Lab Social Neurosciences Research Program is to understand the biological underpinnings of typical and atypical social behavior. This interest is manifested in studies of biological signaling pathways (e.g., oxytocin, vasopressin) that support species-typical social functioning in animals, and how alterations in these systems produce social impairments in primate models and in patients with autism. Our research also tests the effectiveness of promising new medications to enhance social functioning in socially impaired monkeys and in children with autism.

Projects


  • See Lab website for current projects: http://parkerlab.stanford.edu/research/, Stanford University

    Location

    Stanford University; California National Primate Research Center; Caribbean Primate Research Center

    Collaborators

    • Antonio Hardan, Professor, Stanford
    • Joseph Garner, Associate Professor of Comparative Medicine and, by courtesy, of Psychiatry and Behavioral Sciences, School of Medicine
    • Alan Schatzberg, Professor, School of Medicine
    • Jennifer Phillips, Clinical Associate Professor, School of Medicine
    • Joshua Elias, Assistant Professor, Chemical and Systems Biology, School of Medicine
    • Rachel Manber, Professor, School of Medicine
    • Sonia Partap, Clinical Associate Professor, School of Medicine
    • David Lyons, Professor (Research) of Psychiatry & Behavioral Sciences, School of Medicine

2016-17 Courses


Stanford Advisees


Graduate and Fellowship Programs


All Publications


  • Early Predictors of Impaired Social Functioning in Male Rhesus Macaques (Macaca mulatta). PloS one Sclafani, V., Del Rosso, L. A., Seil, S. K., Calonder, L. A., Madrid, J. E., Bone, K. J., Sherr, E. H., Garner, J. P., Capitanio, J. P., Parker, K. J. 2016; 11 (10)

    Abstract

    Autism spectrum disorder (ASD) is characterized by social cognition impairments but its basic disease mechanisms remain poorly understood. Progress has been impeded by the absence of animal models that manifest behavioral phenotypes relevant to ASD. Rhesus monkeys are an ideal model organism to address this barrier to progress. Like humans, rhesus monkeys are highly social, possess complex social cognition abilities, and exhibit pronounced individual differences in social functioning. Moreover, we have previously shown that Low-Social (LS) vs. High-Social (HS) adult male monkeys exhibit lower social motivation and poorer social skills. It is not known, however, when these social deficits first emerge. The goals of this study were to test whether juvenile LS and HS monkeys differed as infants in their ability to process social information, and whether infant social abilities predicted later social classification (i.e., LS vs. HS), in order to facilitate earlier identification of monkeys at risk for poor social outcomes. Social classification was determined for N = 25 LS and N = 25 HS male monkeys that were 1-4 years of age. As part of a colony-wide assessment, these monkeys had previously undergone, as infants, tests of face recognition memory and the ability to respond appropriately to conspecific social signals. Monkeys later identified as LS vs. HS showed impairments in recognizing familiar vs. novel faces and in the species-typical adaptive ability to gaze avert to scenes of conspecific aggression. Additionally, multivariate logistic regression using infant social ability measures perfectly predicted later social classification of all N = 50 monkeys. These findings suggest that an early capacity to process important social information may account for differences in rhesus monkeys' motivation and competence to establish and maintain social relationships later in life. Further development of this model will facilitate identification of novel biological targets for intervention to improve social outcomes in at-risk young monkeys.

    View details for DOI 10.1371/journal.pone.0165401

    View details for PubMedID 27788195

  • Cerebrospinal fluid and plasma oxytocin concentrations are positively correlated and negatively predict anxiety in children MOLECULAR PSYCHIATRY Carson, D. S., Berquist, S. W., Trujillo, T. H., Garner, J. P., Hannah, S. L., Hyde, S. A., Sumiyoshi, R. D., Jackson, L. P., MOSS, J. K., Strehlow, M. C., Cheshier, S. H., Partap, S., Hardan, A. Y., Parker, K. J. 2015; 20 (9): 1085-1090

    Abstract

    The neuropeptide oxytocin (OXT) exerts anxiolytic and prosocial effects in the central nervous system of rodents. A number of recent studies have attempted to translate these findings by investigating the relationships between peripheral (e.g., blood, urinary and salivary) OXT concentrations and behavioral functioning in humans. Although peripheral samples are easy to obtain in humans, whether peripheral OXT measures are functionally related to central OXT activity remains unclear. To investigate a possible relationship, we quantified OXT concentrations in concomitantly collected cerebrospinal fluid (CSF) and blood samples from child and adult patients undergoing clinically indicated lumbar punctures or other CSF-related procedures. Anxiety scores were obtained in a subset of child participants whose parents completed psychometric assessments. Findings from this study indicate that plasma OXT concentrations significantly and positively predict CSF OXT concentrations (r=0.56, P=0.0064, N=27). Moreover, both plasma (r=-0.92, P=0.0262, N=10) and CSF (r=-0.91, P=0.0335, N=10) OXT concentrations significantly and negatively predicted trait anxiety scores, consistent with the preclinical literature. Importantly, plasma OXT concentrations significantly and positively (r=0.96, P=0.0115, N=10) predicted CSF OXT concentrations in the subset of child participants who provided behavioral data. This study provides the first empirical support for the use of blood measures of OXT as a surrogate for central OXT activity, validated in the context of behavioral functioning. These preliminary findings also suggest that impaired OXT signaling may be a biomarker of anxiety in humans, and a potential target for therapeutic development in individuals with anxiety disorders.Molecular Psychiatry advance online publication, 4 November 2014; doi:10.1038/mp.2014.132.

    View details for DOI 10.1038/mp.2014.132

    View details for Web of Science ID 000360175500009

  • Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Parker, K. J., Garner, J. P., Libove, R. A., Hyde, S. A., Hornbeak, K. B., Carson, D. S., Liao, C., Phillips, J. M., Hallmayer, J. F., Hardan, A. Y. 2014; 111 (33): 12258-12263

    Abstract

    The neuropeptide oxytocin (OXT) and its receptor (OXTR) regulate social functioning in animals and humans. Initial clinical research suggests that dysregulated plasma OXT concentrations and/or OXTR SNPs may be biomarkers of social impairments in autism spectrum disorder (ASD). We do not know, however, whether OXT dysregulation is unique to ASD or whether OXT biology influences social functioning more generally, thus contributing to, but not causing, ASD phenotypes. To distinguish between these possibilities, we tested in a child ASD cohort, which included unaffected siblings and unrelated neurotypical controls (ages 3-12 y; n = 193), whether plasma OXT concentrations and OXTR SNPs (i) interact to produce ASD phenotypes, (ii) exert differential phenotypic effects in ASD vs. non-ASD children, or (iii) have similar phenotypic effects independent of disease status. In the largest cohort tested to date, we found no evidence to support the OXT deficit hypothesis of ASD. Rather, OXT concentrations strongly and positively predicted theory of mind and social communication performance in all groups. Furthermore, OXT concentrations showed significant heritability between ASD-discordant siblings (h(2) = 85.5%); a heritability estimate on par with that of height in humans. Finally, carriers of the "G" allele of rs53576 showed impaired affect recognition performance and carriers of the "A" allele of rs2254298 exhibited greater global social impairments in all groups. These findings indicate that OXT biology is not uniquely associated with ASD, but instead exerts independent, additive, and highly heritable influences on individual differences in human social functioning, including the severe social impairments which characterize ASD.

    View details for DOI 10.1073/pnas.1402236111

    View details for Web of Science ID 000340438800080

    View details for PubMedID 25092315