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News

Mother’s immunity linked to brain inflammation in monkeys

by  /  15 November 2014

Anton Watman/Shutterstock.com Monkey, do: People’s immune systems and social behaviors are more like those of macaques than of mice.

Monkeys exposed in utero to their mother’s immune response to a mock infection show inflammation in their brains four years later. Researchers presented the unpublished results today at the 2014 Society for Neuroscience annual meeting in Washington, D.C.

Infections during pregnancy have long been known to increase a woman’s odds of having a child with schizophrenia or autism. In the past few years, researchers have confirmed in mouse models that a mother’s immune response can lead to a wide array of symptoms in her pups, such as anxiety, repetitive burying of marbles, and abnormal vocalizations and social interactions.

“There are, however, limitations in relying solely on rodent models to evaluate risk factors for complex disorders such as autism,” says Melissa Bauman, assistant professor of psychiatry and behavioral sciences at the University of California, Davis, who presented the new findings. Mice and men have dramatically different social and communicative behaviors.

Last year, Bauman and her colleagues debuted a macaque model of maternal immune activation: They injected pregnant monkeys with a mock flu virus at the end of either the first trimester or the second. Both groups of young macaques show stereotyped and repetitive movements by age 2, the study found. Babies exposed during the first trimester also show abnormal social behaviors.

“I was surprised how consistently affected the first-trimester animals were,” Bauman says, especially because primate models, unlike mice, are not genetically identical.

The new study investigated the brain activity of the monkeys at four years old, their age of puberty. These experiments relied on an imaging technology called positron emission tomography, or PET, in which radioactive tracers travel from the animals’ blood to their brains and bind to specific proteins.

Bauman’s team used a tracer called PK11195, which binds to activated microglia, cells associated with brain inflammation that have been linked to autism. Monkeys exposed to an infection in either the first or second trimester show abnormally high levels of inflammation across the whole brain, the study found.

In another experiment, the researchers turned to a tracer called FMT, which is a marker of the synthesis of dopamine, a chemical messenger. Increased levels of dopamine in the striatum, a deep brain region involved in planning and movement, are associated with schizophrenia. And rodent models of maternal infection have shown glitches in dopamine cells, Bauman notes.

The new study found that the brains of the monkeys exposed to maternal infection in the first or second trimester show higher levels of striatal dopamine than in controls.

“We’re pretty excited by these data,” Bauman says. The monkey models “are a nice way to bridge the gap between rodent models and clinical populations.”

What these data don’t yet explain, however, is why exposure during the first trimester, but not the second, leads to social problems reminiscent of autism. “At this point, we’re still searching,” Bauman says.

For more reports from the 2014 Society for Neuroscience annual meeting, please click here.


  • Monideepa

    All this is fine. But what is the remedy.
    Once this fact is established, can then autism be treated with antibiotics as this arising due to germs acquired from the mother. I am a person who has chronic tonsilitis.
    I was unaware as to when i actually conceived, maybe i realised two months later. In this first two months(first trimster) in the evry initial days i had an antibiotic as well as antiworm.Also in the rest of the duration of the pregnancy, I never had any symptom of tonsilitis, though generally i have an infection every 3 months.My 7 year old son has autism. So can i see any ray of hope in this article with regard to a treatment for him.

  • Kellie

    Honest question…not trying to cause an internet riot. If a mock virus and an immune response in the mother can cause autism, why are we pushing vaccines on pregnant women? Wouldn’t that do the same? Not to mention the toxic chemicals involved in vaccines. Mercury is still in multidose flu shots and aluminum is in the dtap and flu. How would a response to a vaccine be different than a natural response to a virus caused by nature?

    • Lisa Boulanger

      Kellie, I agree that this is a very important question to address in future research. We do know that coming down with the flu causes a far more intense immune response than the flu vaccine. The immune challenge being modeled in these experiments is very strong–much more like the real flu than the vaccine, in terms of the intensity of immune response it evokes. In addition, pregnant women are at an increased risk of dying from the flu, due to changes in their immune system associated with pregnancy. While there is no evidence at the moment that the weak immune response evoked by the vaccine causes any problems, it has not yet been exhaustively studied. In the meantime, one option might be for women to get the flu vaccine if they are trying to get pregnant, in order to avoid any concerns they may have about being vaccinated while pregnant, while still protecting them from the risks of a live flu infection during pregnancy.

      Another interesting point is that in humans, for some reason, immune stimulation during pregnancy doesn’t cause problems with brain development nearly as often as it does in animal models. In humans, there is an increase in the risk of autism (or schizophrenia) in the child after maternal infection, but it may only have an effect in genetically predisposed individuals. Many women get the flu during pregnancy and go on to have healthy babies. In animal models, in contrast, fetal brain development is disrupted after maternal immune challenge in more or less every single offspring. One possible reason is that the lab animals tend to be more genetically similar to one another than humans are; another factor is that the exact timing of the immune signal seems to matter; another possible difference is that the experimental immune challenge is quite severe, even in comparison to a live flu infection.

      In short, there’s a lot of research to be done on this topic!

      Lisa Boulanger
      Assistant Professor
      Department of Molecular Biology and Princeton Neuroscience Institute

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