Why you should care
Because autism affects 1 in 68 children — and there are no effective treatments.
“I think of it as the Mount Everest of disorders.” Karen Parker is speaking about autism, a condition that the United Nations estimates affects up to 70 million people worldwide and has no known cure. As a behavioral neuroscientist at Stanford University, Parker, who hikes the Bay Area’s trails with her two Australian Shepherds, knows the challenge before her is steep. But by honing in on the role of hormones like oxytocin and vasopressin in regulating social behavior, she hopes to get purchase on her professional Mount Everest.
An associate professor of psychiatry and behavioral sciences and the director of Stanford’s Social Neurosciences Research Program, Parker published findings last year that indicate that autistic children with low levels of blood oxytocin show improved social functioning when they receive additional oxytocin in the form of a medication. The study was limited to just 32 participants, but her conclusions suggest that children with low oxytocin levels stand to benefit the most from oxytocin treatment, and point the way toward a more personalized approach to treating social deficits in children with autism.
How would I feel if I had a child with a disorder for which there were … no drugs to treat the core symptoms?
Parker, a Boulder, Colorado, native who grew up in suburban Chicago, traces her early interest in science to her father, an electrical engineer who worked for Bell Laboratories in its golden age. That gave her a front seat to cutting-edge science and engineering research, she says. Her aunt, who had a Ph.D. in communication disorders, also discussed her research with young Parker. “It was really exciting to see the research arc from an idea, to the design of a project, to the execution, to the new data,” she says.
That early exposure to science led Parker, now 46, to pursue a research career. As an undergraduate at the University of Michigan, she became interested in how social bonds are formed among humans and other animals and studied neuroscience to understand the biological basis of social functioning. In grad school at U of M, she studied oxytocin and vasopressin in meadow voles (mouse-like creatures) — leading her to question how impairment of these naturally occurring hormones might tell us more about human disorders like autism, a condition characterized by social impairments such as difficulty in communicating and forming relationships.
Parker arrived at Stanford in 2001 to train in the psychiatry department as a postdoctoral fellow. Her timing was fortuitous, as the university was in the process of establishing an autism research center, and Parker was recruited to stay on as a faculty member. She lasered in on autism research, aware that the field was surprisingly underdeveloped considering the size of the population affected by the disorder. With no promising diagnostics or therapies, she says, “it felt like there was this canvas that was empty.”
It was around the same time that Parker became a first-time parent — she now has three healthy children — and she came to know the families of children with autism. “How would I feel if I had a child with a disorder for which there were no objective laboratory-based diagnostics and no drugs to treat the core symptoms?” She became “consumed” with searching for answers that could substantially improve pediatric health.
Revisiting her work on hormones that influence social functioning, Parker began to investigate whether oxytocin played a role in autism. She discovered that on average, people with and without autism had the same blood oxytocin levels. But in the subset of people with autism and very low oxytocin levels, administering oxytocin improved their social functioning. She’s now looking at vasopressin, a hormone similar to oxytocin but one that’s more important to male social functioning (boys are nearly five times more likely than girls to have autism).
In addition, Parker is collaborating with the California National Primate Research Center at UC Davis to study macaque monkeys that have naturally occurring social impairments. Genetically modified mouse models for autism exist, Parker explains, but they don’t have the same neural circuitry or show the same behaviors as human patients; consequently, many of the behavioral tests in rodents have little relevance to humans.
“We need to have models to understand the biology [of autism], and that’s why the work she’s doing is so important,” says Elliott Sherr, professor of neurology at UCSF. Because the work is still in the early stages, Parker has yet to identify all the ways in which the monkeys differ from humans in terms of social behavior — an essential piece to unpack, Sherr adds.
As a first step toward running clinical trials in human patients, Parker plans to test new therapeutic compounds (such as hormone-based or pharmacological treatments) in monkeys to establish that they’re safe. “The way that I’ve set the lab up is that we do a lot of parallel work in our monkey model and our human patients so that we can readily translate findings that we see in the animals to the patients,” she says.
It’s an approach that sets her apart. “She is really one of only a handful of people who are doing comprehensive translational research that directly tries to take knowledge gained in animal models and apply it in human beings,” says Michael Platt, a professor of psychology at the University of Pennsylvania.
Parker also makes sure to regularly step outside her lab and glean insights from parents of children with autism. “I’ve had a lot of parents come up and tell me things like, ‘I got a dog and my kid has dramatically improved,’ or ‘my kid has done equine therapy and they’ve dramatically improved.’” She knows, of course, that these are anecdotal observations, but she uses them to seed new studies. Perhaps, she muses, playing with a dog or interacting with a horse might cause autistic kids to produce more oxytocin or vasopressin.
Long drawn to scientific inquiry, Parker says she got involved in autism research because it seemed like such an intricate puzzle. But the more she learned, and put faces to the disorder, “the more I became motivated to find answers.” She’s still climbing, in other words.