Researchers at ETH Zurich have found a way to influence the development of schizophrenia-like behavioural patterns in mice through a combination of infection during pregnancy and stress at puberty.
Schizophrenia is an incurable mental disorder that affects one per cent of the population. Symptoms of the disorder typically manifest in adulthood, but scientists have long suspected that environmental factors such as stress and pathogens during development may be important risk factors for the disorder.
Urs Meyer’s research group subjected mice to two different environmental influences. The first was an infection in the mother during the first half of the pregnancy to provoke an immune response. Thirty to 40 days after birth, at a time equivalent to mouse puberty, the mice were exposed to five different stressors as a second environmental influence. Control mice were either exposed to one or none of the environmental influences.
Researchers then tested the mice’s behaviour and found that the mice who experienced both infection and stress had far more behavioural abnormalities akin to schizophrenia in humans than either of the control groups.
The study hypothesized that the infection activated immune cells in the nervous system of the fetus which produced cytotoxins that alter brain development. These microglial immune cells lie dormant after the infection subsides, but can be activated again through a powerful and prolonged stressor, causing neuroimmunological changes that are not evident until adulthood.
Either of the influences alone, infection or pregnancy, are not enough to lead to the development of schizophrenia. Rather it is the combination of influences at the right time that seems to be the key to the disorder. This study concludes that schizophrenia may be stopped by taking preventive action at appropriate times.
With files from ScienceDaily