Research ArticlePsychiatry

Arginine vasopressin in cerebrospinal fluid is a marker of sociality in nonhuman primates

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Science Translational Medicine  02 May 2018:
Vol. 10, Issue 439, eaam9100
DOI: 10.1126/scitranslmed.aam9100

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Shedding light on social behavior in primates

Autism is a brain disorder characterized by core social impairments that are difficult to model in animals. Now, Parker and colleagues have developed a monkey model of naturally occurring low sociality. They use their monkey model to identify differences in neuropeptide and kinase signaling pathways between low- and high-social monkey groups. The authors report that arginine vasopressin (AVP) in cerebrospinal fluid (CSF) was a key marker of sociality in the monkey cohort. They then measured AVP in CSF from seven children with autism and seven children without autism (but with other medical conditions) and found lower concentrations of CSF AVP in the children with autism. The new findings suggest that the AVP signaling pathway warrants consideration in future research that aims to develop new drugs and diagnostics for autism.


Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by core social impairments. ASD remains poorly understood because of the difficulty in studying disease biology directly in patients and the reliance on mouse models that lack clinically relevant, complex social cognition abilities. We use ethological observations in rhesus macaques to identify male monkeys with naturally occurring low sociality. These monkeys showed differences in specific neuropeptide and kinase signaling pathways compared to socially competent male monkeys. Using a discovery and replication design, we identified arginine vasopressin (AVP) in cerebrospinal fluid (CSF) as a key marker of group differences in monkey sociality; we replicated these findings in an independent monkey cohort. We also confirmed in an additional monkey cohort that AVP concentration in CSF is a stable trait-like measure. Next, we showed in a small pediatric cohort that CSF AVP concentrations were lower in male children with ASD compared to age-matched male children without ASD (but with other medical conditions). We demonstrated that CSF AVP concentration was sufficient to accurately distinguish ASD cases from medical controls. These data suggest that AVP and its signaling pathway warrant consideration in future research studies investigating new targets for diagnostics and drug development in ASD.

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