Non-human primate model of the maternal infection risk factor for autism and schizophrenia

Untitled-1We have just published our first paper on extending the rodent model of maternal immune activation to monkeys. As repeat readers of this blog, and the accompanying book, well know, an important risk factor for both autism and schizophrenia is infection during pregnancy. We modeled this in mice by simply activating the mother’s immune system at mid-pregnancy. The resulting offspring display behaviors consistent with both of these disorders as well as neuropathology seen in these disorders. Since monkey brains and behavior more closely resemble humans than do mice, it was important to test whether the same findings would hold true when activating the immune system during pregnancy in monkeys.

Spearheading this work at UC Davis and the California Regional Primate Center, Melissa Bauman and David Amaral found that, indeed, the cardinal symptoms of autism (stereotyped/repetitive behavior, deficits in verbal communication, and highly abnormal social behaviors) are found in the offspring of mothers immune activated during either the first or second trimester, although more pronounced effects were seen in the former offspring. In further work yet to be published, we also found that there are eye tracking abnormalities (lack of eye contact with others) in these offspring, as is seen in human autism. These findings not only establish a new model in non-human primates, but they also validate prior work with rodents: the latter findings are not restricted just to mice and rats.

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13 Responses to Non-human primate model of the maternal infection risk factor for autism and schizophrenia

  1. Hi Paul Patterson –

    I feel really bad for those poor little monkeys!

    My squeamishness aside, my analytic side begins to wonder when/if some physiological *differences* are going to be evaluated for; i.e., amygdala sizes, signs of peripheral/CNS immune dysregulation, intestinal permeability, etc?

    Great work. Keep it up!

  2. Natasa says:

    This is exciting, thank you! Are there are any plans of ‘treatment trials’ in this monkey model?

  3. John says:

    Another piece of the puzzle: Influenza A infection causes Strep pneumo bacteria to breakup their biofilm and cause secondary infection (and, presumably, immune response). This is interesting because PANDAS kids (or whatever the name is these days) have their symptom flares (OCD or tics and anxiety, etc) after viral infections, thus confounding their physicians and seemingly betraying their diagnoses. A paradox resolved?


  4. Hi Paul

    I thought this might be of interest –

    Scientists closer to universal flu vaccine after pandemic “natural experiment”

    immune correlates of protection against symptomatic pandemic influenza. Nature Medicine, 2013; DOI: 10.1038/nm.3350

    “They found that those who fell more severely ill with flu had fewer CD8 T cells in their blood, and those who caught flu but had no symptoms or only mild symptoms had more of these cells.”

    “We already know how to stimulate the immune system to make CD8 T cells by vaccination. Now that we know these T cells may protect, we can design a vaccine to prevent people getting symptoms and transmitting infection to others. This could curb seasonal flu annually and protect people against future pandemics.”

    I wonder if this might have treatment / preventative implications for maternal immune activation animal models ?

  5. Hi Paul

    Had to pass this on directly as it has lots of themes from your book
    Full Paper at link

    Norbert Müller
    Department of Psychiatry and Psychotherapy, Ludwig-Maximilian University Munich, Munich, Germany…/dnb_vol25_no3_292.pdf

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