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      Arginine Vasopressin Is a Blood-Based Biomarker of Social Functioning in Children with Autism

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          Abstract

          Brain arginine vasopressin (AVP) critically regulates normative social behavior in mammals, and experimental disruption of the AVP signaling pathway produces social impairments in rodent models. We therefore hypothesized that AVP signaling deficits may contribute to social impairments in children with autism spectrum disorder (ASD). Since blood measures (which are far easier to obtain than brain measures) of AVP are most meaningful if they are related to brain AVP activity, Study 1 tested the relationship between AVP concentrations in concomitantly collected blood and CSF samples from children and adults (N = 28) undergoing clinical procedures. Study 2 tested whether blood AVP concentrations: 1) differed between children with ASD (N = 57), their ASD discordant siblings (N = 47), and neurotypical controls (N = 55); and 2) predicted social functioning (using the NEPSY-II Theory of Mind and Affect Recognition tasks and the Social Responsiveness Scale) in this large, well-characterized child cohort. Blood AVP concentrations significantly and positively predicted CSF AVP concentrations ( F 1,26 = 7.17, r = 0.46, p = 0.0127) in Study 1. In Study 2, blood AVP concentrations did not differ between groups or by sex, but significantly and positively predicted Theory of Mind performance, specifically in children with ASD, but not in non-ASD children ( F 1,144 = 5.83, p = 0.017). Blood AVP concentrations can be used: 1) as a surrogate for brain AVP activity in humans; and 2) as a robust biomarker of theory of mind ability in children with ASD. These findings also suggest that AVP biology may be a promising therapeutic target by which to improve social cognition in individuals with ASD.

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          Most cited references 23

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          Oxytocin, vasopressin, and the neurogenetics of sociality.

           Z Donaldson,  L Young (2008)
          There is growing evidence that the neuropeptides oxytocin and vasopressin modulate complex social behavior and social cognition. These ancient neuropeptides display a marked conservation in gene structure and expression, yet diversity in the genetic regulation of their receptors seems to underlie natural variation in social behavior, both between and within species. Human studies are beginning to explore the roles of these neuropeptides in social cognition and behavior and suggest that variation in the genes encoding their receptors may contribute to variation in human social behavior by altering brain function. Understanding the neurobiology and neurogenetics of social cognition and behavior has important implications, both clinically and for society.
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            The challenge of translation in social neuroscience: a review of oxytocin, vasopressin, and affiliative behavior.

             Thomas Insel (2010)
            Social neuroscience is rapidly exploring the complex territory between perception and action where recognition, value, and meaning are instantiated. This review follows the trail of research on oxytocin and vasopressin as an exemplar of one path for exploring the "dark matter" of social neuroscience. Studies across vertebrate species suggest that these neuropeptides are important for social cognition, with gender- and steroid-dependent effects. Comparative research in voles yields a model based on interspecies and intraspecies variation of the geography of oxytocin receptors and vasopressin V1a receptors in the forebrain. Highly affiliative species have receptors in brain circuits related to reward or reinforcement. The neuroanatomical distribution of these receptors may be guided by variations in the regulatory regions of their respective genes. This review describes the promises and problems of extrapolating these findings to human social cognition, with specific reference to the social deficits of autism. (c) 2010 Elsevier Inc. All rights reserved.
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              Promoting social behavior with oxytocin in high-functioning autism spectrum disorders.

              Social adaptation requires specific cognitive and emotional competences. Individuals with high-functioning autism or with Asperger syndrome cannot understand or engage in social situations despite preserved intellectual abilities. Recently, it has been suggested that oxytocin, a hormone known to promote mother-infant bonds, may be implicated in the social deficit of autism. We investigated the behavioral effects of oxytocin in 13 subjects with autism. In a simulated ball game where participants interacted with fictitious partners, we found that after oxytocin inhalation, patients exhibited stronger interactions with the most socially cooperative partner and reported enhanced feelings of trust and preference. Also, during free viewing of pictures of faces, oxytocin selectively increased patients' gazing time on the socially informative region of the face, namely the eyes. Thus, under oxytocin, patients respond more strongly to others and exhibit more appropriate social behavior and affect, suggesting a therapeutic potential of oxytocin through its action on a core dimension of autism.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                22 July 2015
                2015
                : 10
                : 7
                Affiliations
                [1 ]Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California, 94305, United States of America
                [2 ]Department of Comparative Medicine, Stanford University School of Medicine, Stanford, California, 94305, United States of America
                [3 ]Department of Pediatrics, Division of Pediatric Hematology, Oncology, SCT and Cancer Biology, Stanford University School of Medicine, Stanford, California, 94305, United States of America
                [4 ]Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, 94305, United States of America
                Hamamatsu University School of Medicine, JAPAN
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: DSC SP JMP AYH KJP. Performed the experiments: DSC SAH RAL SWB KBH LPJ RDS SLH SP JMP AYH KJP. Analyzed the data: DSC CLH JPG KJP. Contributed reagents/materials/analysis tools: SAH. Wrote the paper: DSC JPG SAH RAL SWB KBH LPJ RDS CLH SLH SP JMP AYH KJP. Secured funding for the studies: KJP AYH DSC SP.

                Article
                PONE-D-15-16226
                10.1371/journal.pone.0132224
                4511760
                26200852

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                Page count
                Figures: 2, Tables: 2, Pages: 14
                Product
                Funding
                This research was supported by a Simons Foundation Autism Research Initiative Pilot Award (#93231), the National Institutes of Health (R21MH100387; UL1 RR025774; RR000167), the Katherine D. McCormick Fund, the Mosbacher Family Fund for Autism Research, Stanford's Bio-X NeuroVentures Program, the Weston Havens Foundation, the Stanford University Child Health Research Institute, an Autism Speaks Meixner Fellowship in Translational Research (#7895), and a Stanford University School of Medicine Dean's Postdoctoral Fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Custom metadata
                Data from Study 1 are freely available and included in Table 1. However, publicly releasing the detailed information from Study 2’s dataset presents a risk to participant confidentially and may constitute a privacy violation for study participants. Data will therefore be available upon request to qualified investigators by contacting the corresponding author, Dr. Karen Parker ( kjparker@ 123456stanford.edu ).

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