For the environmental animal model I employed a wellestablished experimental mouse model of prenatal exposure to a viral-like acute phase response induced by the synthetic analogue of double-stranded ribonucleic acid, polyriboinosinic-polyribocytidilic acid (Poly-I:C). Whereas for the genetic model I used a double transgenic mouse model with an inducible expression system of mutant human Disrupted-in-Schizophrenia-1 (DISC1). In this respect, DISC1 has emerged as a strong candidate gene associated with major mental illness including depression, anxiety, bipolar disorder and schizophrenia.What's the point of the research?
The prevailing hypothesis for the etiology of schizophrenia is that variations in multiple risk genes, each contributing a subtle effect, interact with each other and with environmental stimuli to impact both early and late brain development. Although a clear mechanism underlying the pathogenesis of schizophrenia remains unknown, maternal immune activation as a consequence of exposure to infection during pregnancy has become an attractive hypothesis for explaining, at least in part, the pathophysiology of schizophrenia.