Credit: Kathy West
For years, Catherine Talbot de Florida Tech, assistant professor of psychology, has worked to understand the sociality of male Rhesus monkeys and how little social monkeys can serve as a model for autistic humans. Its most recent conclusions show that the reconstruction of a deficient hormone, vasopressin, helped the monkeys to become more social without increasing their aggression – a discovery that could change the treatment of autism.
Currently, the centers for Disease Control and Prevention reports that a in 36 child in the United States is affected by autistic spectrum disorder (TSA). This is an increase compared to one in 44 children reported in 2018. There are currently two treatments approved by the FDA, said Talbot, but they only deal with associated symptoms, not from the TSA root. The boost of prevalence and consciousness of the disorder arouses the following question: what is the cause?
Some rhesus monkeys are naturally weak, which means that they demonstrate bad social cognitive skills, while others are very social. Their individual variation in sociality is comparable to the way in which human sociality varies, ranging from people that we consider social butterflies to those who are not interested in social interactions, similar to certain people diagnosed with a TSA, said Talbot. Its objective was to understand how variations in biology and behavior influence social cognition.
In a research article published in the journal PNA Titled “Nebulized Vasopressin Penetraes CSF (Cerebral Spinal Fluid) and Improves Social Cognition Without Inducing Aggression In A Rhesus Monkey Model of Autism,” Talbot and Researchers with Stanford, The University of California, Davis and the California National Research Center Vasopressin, a hormone that is know to contribute to mammalian social behavior, as a potential therapeutic treatment that may in the end, help people with autistic people to work better in society.
Previous work in this research group has discovered that vasopressine levels are lower in their low Rhesus monkey model, as well as in a limited group of people with ASD.
Previous studies testing vasopressin in rodents have shown that the increase in hormone levels caused more attack. Consequently, the researchers warned against the administration of vasopressin as treatment, said Talbot. However, it argued that in these studies, vasopressin has induced an aggression in contexts where aggression is the socially appropriate response, such as watchtocks in their territory of origin, so that the hormone can promote typical behavior of species.
She also noted that previous studies had tested vasopressin in “neurotypical” rodents, as opposed to animals with weak social tendencies.
“It may be that individuals with the lowest levels of vasopressin benefit the most, that is to say the step towards precision medicine that we must now study,” said Talbot.
In his latest article, Talbot and his co-authors tested how low social monkeys with low levels of vasopressin and a high autism overhaul have responded to vasopressin supplementation to compensate for their natural deficiency. They administered the hormone through a nebulizer in which the monkeys could opt. For a few minutes a week, the monkeys voluntarily held their faces to a nebulizer to receive their dose while sipping white grape juice – a favorite among the monkeys, said Talbot.
After administering the hormone and verified that he increased the levels of vasopressin in the central nervous system, the researchers wanted to see how the monkeys responded to both affiliated and aggressive stimuli by showing them videos describing these behaviors. They also compared their ability to recognize and remember new objects and faces, which is another important social competence.
They found that the normally Bas-Social monkeys do not respond to social communication and were better to recognize and remember objects in relation to faces, similar to certain humans diagnosed with a TSA. When the monkeys received vasopressin, they started to seek affiliated and pro-social behaviors, but not to aggression. He also improved their facial recognition memory, which makes him equivalent to their object recognition memory.
In other words, vasopressin has “saved” the capacity of low social monkeys to respond to others and to remember new faces. The treatment has succeeded – vasopressin selectively improved the social cognition of these little social monkeys.
“It was really exciting to see it materialize after having devoted so much work in this project and overcoming so many challenges,” said Talbot about his conclusions.
One of Talbot’s co-authors has already started to translate this work into cohorts of autistic patients. It expects more clinical trials to follow.
In the immediate future, Talbot examines how other more complex social cognitive capacities such as the theory of the mind – the ability to take the perspective of another – can differ in little social monkeys compared to more social monkeys and how it relates to their underlying biology.
Beyond that, Talbot hopes that they will be able to target young monkeys who risk developing autism social deficits for the treatment of vasopressin, to see if an early intervention could help change their development trajectory and ultimately translate this therapy into targeted human trials.
More information:
Catherine F. Talbot et al, nebulized vasopressin enters the CSF and improves social cognition without inducing an aggression in a model of Autism Rhesus monkey, Proceedings of the National Academy of Sciences (2024). DOI: 10.1073 / PNAS.2418635121
Supplied by the Florida Institute of Technology
Quote: Hormonal supplementation in rhesus monkeys indicates the potential autism treatment (2025, April 28) recovered on April 28, 2025 from
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