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Features / Webinars

Jonathan Kipnis on microglia and therapeutic targets

27 March 2013
The Presenter
Presenter

Jonathan Kipnis

Professor of Neuroscience, University of Virginia

Jonathan Kipnis is professor of neuroscience at the University of Virginia. He seeks to understand the complex interactions between the immune and nervous systems.

On 27 March, Jonathan Kipnis explained how microglia and peripheral immunity may affect the pathology of neurodevelopmental disorders, opening the door for new therapeutic possibilities.

You can watch a complete replay of the webinar above.

Use the comments section below to submit questions we didn’t have time to discuss during the Q&A session, or to pose follow-up questions. Kipnis, who is professor of neuroscience at the University of Virginia School of Medicine in Charlottesville, Virginia, will monitor this thread.

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The Spectrum Webinar Series aims to facilitate the free exchange of ideas among autism researchers, including discussion of published and unpublished research, hypotheses and results. Members of the press may report information presented during a Spectrum webinar only if that material has already been published elsewhere or they have first obtained express written consent from the presenter.

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Presentations by leading experts that showcase new findings, useful techniques and emerging topics in autism research. We invite questions before and during the presentations in the Comments section.
  • Kathryn Condon

    Did you perform the reverse experiment — replace WT immune system with MECP2 -/Y bone marrow — to help determine which Rett symptoms are due to immune system dysfunction (could also inform developmental timeline?)?

    • J Kipnis

      This is a very good question and we are addressing it now using genetic tools, which will allow us a better resolution of symptoms, as compared to BMT approach.

  • Portia McCoy

    Based on your presentation, it would seem that pharmacological treatments that rescues MeCP2 expression solely in microglia should be sufficient to rescue many aspects of the disease in model mice. You mentioned that MeCP2 expression is lower in microglia than neurons, is there a downside to overexpression of MeCP2 in microglia?

    • J Kipnis

      This is another great question. We are not aware of any pharmacological agent that can increase mecp2 (do you know any?) but your point that maybe overexpressing it in microglia will not be as devastating as its overexpression in neurons, is very well taken. We are collaborating with another researcher at our University, to address this exact question.

  • Branka Novakovic

    Did you try replacement of microglia in female mice?

    • J Kipnis

      Hi Branka. Yes, we did perform BMT in females, and it was actually published in our original manuscript last year. Sorry I did not present this data but I wanted to talk about too many things and only had about 50 min for the lecture. The effect in the females was mainly on their behavior and appearance (breathing, weight, fur condition, motor function, etc). As you know female mice do not die from this disease, so there was no life extension, but overall most of the symptoms were improved.

  • Natasa

    Has it been considered/ruled out that the higher use of NSIAD amongst those people who developed dementia could simply be a reflection, a downstream (rather than causative) effect of underlying immune pathology lowering pain threshold and causing milder health problems? For example if immune problems, that later on cause visible dementia, are present and causing health issues such as frequent migraine/headache and similar, the sufferer would be more likely to take NSAIDS. When the sufferer later on develops dementia, it could not be caused/related to NSAIDS, but to underlying pathology that led to their heavier use of NSAIDS in the first place. Has this been ruled out?

    • J Kipnis

      Thank ou for your question and your concern is well taken. By no mean I wanted to say that this study proves our hypothesis, but this is another piece to the puzzle that maybe will help to see a bigger picture. Right now our studies are all done in mice and any piece of relevance from humans that supports our theory is of course exciting for us, hence I mentioned it in my talk. As you may know, families that have kids with autism often report that during illness such as cold or flu, the neurological symptoms are improved. We think this is because immunity is hyper functioning during the illness and as “side effect” benefits the brain – this is not a proof of course to anything we suggest but again another piece of evidence that goes along the line of our research in rodents.

  • M Georges

    NSAIDs inhibit microglial activation, they don’t make it worse.

    • J Kipnis

      I do not know what is the direct effect of NSAID on microglia activation and how well the active compounds actually penetrate the BBB. Microglia “activation” could be of many “flavors” – some of which may benefit and other may disturb the brain function. Looking only at “activation” markers without further deciphering the “flavor” will not suffice to understand the role of these cells in brain function. In my simplistic philosophy – if these cells (microglia) are in the brain they must be there for a good reason!

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