The interplay between an infection during pregnancy and stress in puberty plays a key role in the development of schizophrenia, behaviourists from ETH Zurich demonstrated in a mouse model.
Around one percent of the population suffers from schizophrenia, a serious mental disorder that usually does not develop until adulthood and is incurable. Psychiatrists and neuroscientsists have long suspected that adverse environmental factors play an important role in causing schizophrenia.
Prenatal infections such as toxoplasmosis or influenza, psychological stress or family history have all come into question as risk factors. Until now, researchers were unable to identify the interplay of the individual factors linked to this serious mental disease.
A research group headed by Urs Meyer, a senior scientist at the Laboratory of Physiology and Behaviour at ETH Zurich, has now made a breakthrough: for the first time, they were able to find clear evidence that the combination of two environmental factors contributed significantly to the development of schizophrenia-relevant brain changes, according to a report in Science Daily.
The researchers developed a special mouse model, with which they were able to simulate the processes in humans, virtually in fast-forward mode.
"Only one of the factors -- namely an infection or stress -- is not enough to develop schizophrenia," underscores Meyer.
The infection during pregnancy lays the foundation for stress to "take hold" in puberty. The mother's infection activates certain immune cells of the central nervous system in the brain of the foetus, microglial cells, which produce cytotoxins that alter brain development of the unborn child.