A Review of the Foetal Brain Cytokine Imbalance Hypothesis of Schizophrenia
Maternal infection during pregnancy increases the risk of schizophrenia and other brain disorders of neurodevelopmental origin in the offspring. A multitude of infectious agents seem to be involved in this association. Therefore, it has been proposed that factors common to the immune response to a wide variety of bacterial and viral pathogens may be the critical link between prenatal infection and postnatal brain and behavioural pathology. More specifically, it has been suggested that the maternal induction of pro-inflammatory cytokines may mediate the neurodevelopmental effects of maternal infections. Here, we review recent findings from in vitro and in vivo investigations supporting this hypothesis and further emphasise the influence of enhanced anti-inflammatory cytokine signaling on early brain development. Disruption of the foetal brain balance between pro- and anti-inflammatory cytokine signaling may thus represent a key mechanism involved in the precipitation of schizophrenia-related pathology following prenatal maternal infection and innate immune imbalances.
Meyer U, Feldon J, Yee BK. A Review of the Fetal Brain Cytokine Imbalance Hypothesis of Schizophrenia. Schizophr Bull. 2008 Apr 11. View Abstract View Full Paper
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Keywords:cytokines, foetal, neurodevelopmental, pregnancy, schizophrenia
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The immune system is prone to the same grave misfortunes as any defense system handling weapons: collateral damage that comes with the destruction of the enemy on one’s own territory and friendly fire due to mistaken identity. Whereas the collateral damage is the price we pay for clearance of infections, autoimmunity is a pathological process. Nevertheless, the effector mechanisms involved in both processes are the same. Whether environment can be a cause, a trigger or an amplifier of an autoimmune disease are questions that are being intensively investigated.
