New results presented at the 2011 meeting of the Society of Neurosience

Given that some 32,000-odd (and some not so odd) researchers attended this annual meeting in Washington DC, it is difficult to summarize all the relevant and interesting findings. Nonetheless, here is a brief effort on some of the highlights:

Alan Brown (Columbia College of Physicians and Surgeons; brief biography in my book) presented new results linking maternal infection with elevated risk for bipolar disorder in the offspring.  The highest risk appears to be infections in the 2nd and 3rd trimesters. This is a different time window than that found for the risk of maternal infection in schizophrenia (late 1st, early 2nd highest risk). The particular infection documented in this new work is influenza.

Carlos Pardo (Johns Hopkins; also brief bio in my book) presented evidence of increased immune cell invasion of the cerebral spinal fluid (CSF) in autism subjects with regression (versus autism subjects without regression). This gives these cells closer access to the brain. How the cells got passed the blood brain barrier, and what they are doing in the CSF is unknown at this point, but this finding further supports the rapidly accumulating evidence of immune involvement in this disorder. A far more comprehensive summary of interesting findings presented at this meeting regarding autism can be found on the SFARI website. A summary of Rett syndrome presentations at the meeting can be found on the IRSF site.

L. Schwieler (Linkopings U, Sweden) reported significantly increased levels of the pro-inflammatory cytokine IL-6 in the CSF of chronic schizophrenia subjects. S. Fillman (U of New South Wales, Australia) finds strongly increased levels of RNAs for several inflammatory cytokines (including IL-6) in schizophrenia brains, extending prior reports of immune dysregulation in postmortem brains.

T. Town (Cedars Sinai Hospital, Los Angeles) noted that some 25 (!) epidemiological studies have shown that people with a history of prolonged use of non-steroidal anti-inflammatory drugs have a decreased risk for Alzheimer’s disease (AD). He presented evidence of inflammation in a rat model of AD, and made the point that targeting the inflammatory molecule CD45 may be a good approach for therapy.

Rene Hen (Columbia) summarized findings on production of new neurons in the adult mouse hippocampus. 3,000 new neurons are produced there each day, but 80% of them die by the end of the first month. Stress lowers production and survival of these new neurons, while enriching the environment of the mice increases production and survival. Treating the mice with anti-depression drugs (SSRIs) greatly increases new neuron production in part of the hippocampus, and in an amazing experiment, Hen showed that stimulating/activating these new neurons had an anti-anxiolytic effect on the behaivor of the mice – they are much more likely to move into open areas that they were previously afraid to enter.

New results were presented by Melissa Bauman (U Calif at Davis) on a non-human primate model of the maternal infection risk factor. This experiment extends our work on mice to a more human-like model. She finds that young offspring of mothers given an immune stimulation (mimicking maternal infection) during the 2nd trimeter are much more likely than controls to exhibit tantrums and self-soothing behaviors. Moreover, offspring from 1st and 2nd trimester immune activation mothers are much more likely than controls to exhibit repetitive and stereotyped behaviors analogous to those seen in autism. In human studies, maternal infection is linked to increased risk for autism in the offspring (see Chap. 5 of my book). Establishing a non-human primate model of this risk factor will enable important studies of the development of human-like, abnormal behaviors as well as raising the potential for testing human-relevant treatments.

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