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Annotation

Meyer U, Nyffeler M, Engler A, Urwyler A, Schedlowski M, Knuesel I, Yee BK, Feldon J. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. J Neurosci . 2006 May 3 ; 26(18):4752-62. PubMed Abstract

Comments on Paper and Primary News
Primary News: Bad Timing: Prenatal Exposure to Maternal STDs Raises Risk of Schizophrenia

Comment by:  Paul Patterson
Submitted 22 May 2006 Posted 22 May 2006

Over the past six years, Alan Brown and colleagues have published an impressive series of epidemiological findings on schizophrenia in the offspring of a large cohort of carefully studied pregnant women (reviewed by Brown, 2006). Their work has confirmed and greatly extended prior findings linking maternal infection in the second trimester with increased risk for schizophrenia in the offspring. Moreover, Brown et al. found an association between anti-influenza antibodies in maternal serum and increased risk for schizophrenia, as well as a similar association with elevated levels of a cytokine in maternal serum. In a new paper (Babulas et al., 2006), this group reports a fivefold increase in risk for schizophrenia spectrum disorders in the offspring of women who experienced a genital/reproductive infection during the periconception period. The infections considered were endometritis, cervicitis, pelvic inflammatory...  Read more


View all comments by Paul Patterson

Primary News: Bad Timing: Prenatal Exposure to Maternal STDs Raises Risk of Schizophrenia

Comment by:  Jürgen Zielasek
Submitted 3 June 2006 Posted 3 June 2006

Meyer and coworkers provide interesting new data on the role of the immune system in mediating the damage caused by viral infections during pregnancy on the developing nervous system of the fetus. Not just the timing of the infection appears to be critical, but the developing fetal immune system appears to play a role, too.

Polyinosinic-polycytidylic acid (polyI:C), which was employed by Meyer et al., is frequently used to mimic viral infections. It is a synthetic double-stranded RNA and has adjuvant-effects (Salem et al., 2005). PolyI:C binds to target cells via the "Toll-like receptor 3" (TLR3). TLR3 serves as a receptor in trophoblast cells and uterine epithelial cells mediating local immune activation at the maternal-fetal interface after viral infections (Abrahams et al., 2005; Schaefer et al., 2005). Glial cells like microglia and...  Read more


View all comments by Jürgen Zielasek

Comment by:  Akira Sawa, SRF Advisor
Submitted 5 June 2006 Posted 5 June 2006

I was greatly interested to read the recent article by Benjamin Yee and colleagues. In this article, the authors hypothesized that cytokine-associated inflammatory responses would be important for maternal infection-induced neuropsychiatric conditions. Thus, the authors administered the viral mimic polyriboinosinic-polyribocytidylic acid (polyI:C) into pregnant mouse dams on gestational day 9 or day 17 and examined the effects in the offspring. It is very impressive that an acute insult, depending on the embryonic day, leads to varied brain changes, as well as behavioral alterations, even in adulthood.

One important lesson from this study is how critical it is to use appropriate molecular markers (in this case, caspase-3, reelin, etc.) in dissecting anatomical and histological changes that may potentially occur in animal models for psychiatric conditions. The data clearly indicate that classic Nissl staining is insufficient to detect important molecular changes that may underlie behavioral alterations in these animals. Many laboratories are now generating and...  Read more


View all comments by Akira Sawa
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