s of newly born neurons in the dentate gyrus of the hippocampus, but only the mice treated later in gestation displayed significantly elevated levels of caspase activation and apoptosis of neurons. The mice also showed different patterns of maternal and fetal production of proinflammatory and anti-inflammatory cytokines, depending on the timing of polyI:C injection.
These results suggest that the same inflammatory stimulus, when present at different gestational stages, can interfere with distinct developmental pathways via stimulation of varying cytokine profiles. If these results translate to humans, then timing of infection and the cytokines induced should be a critical determinant of the type of pathology that shows up in adulthood. This jibes with the current epidemiological study, and previous ones using the same group of patients (Brown et al., 2001; Brown et al., 2004), that link the risk for schizophrenia to infections occurring in a window of vulnerability in early to mid-pregnancy.—Pat McCaffrey.
Babulas V, Factor-Litvak P, Goetz R, Schaefer CA, Brown AS. Prenatal exposure to maternal genital and reproductive infections and adult schizophrenia. Am J Psychiatry. 2006 May;163(5):927-9. Abstract
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. Abstract