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1) Various studies point to genetic factors, poor nutrition, fetal development, birth complications, immune reactions, and toxins. They also suggest that brain abnormalities may result from exposure to viruses before birth. The viruses enter the fetus' brain and interrupt proper brain development, OR the viruses remain quiet until puberty or young adulthood, activated by changes in hormones or by another viral infection, and help to bring about schizophrenic symptoms.

2) Animal model investigations, found that an unusually large number of people with schizophrenia are born during the winter. The winter birth rate among people with schizophrenia is 5 to 8 percent higher than among other people. This could be because of an increase in fetal or infant exposure to viruses at that time of year.

3) Investigations of fingerprints. People with schizophrenia often have significantly more or fewer ridges than their nonschizophrenic identical twins. Fingerprints form in the fetus during the 2nd trimester, when the fetus is most vulnerable to certain viruses. The fingerprint irregularities of some people with schizophrenia could reflect a viral infection contracted during the prenatal period, an infection that also predisposed the individuals to schizophrenia.

4) Studies show mothers of schizophrenic children were more likely to have been exposed to the influenza virus during pregnancy than were mothers of people without schizophrenia.

5) Other studies have found antibodies to certain viruses, incl. viruses usually found in animals, in the blood of 40% of research participants with schizophrenia. The presence of such antibodies suggests that these people had at some time been exposed to those particular viruses.
Schizophrenia involves an over-reactivity of dopamine transmission in the brain.

The major source of evidence for the dopamine model is found in the effects of antipsychotic drugs called neuroleptics. This theory is based on the effectiveness of the medications.

Over past 4 decades, researchers developed this hypothesis to explain findings. Certain neurons using dopamine fire too often, producing symptoms of schizophrenia.

The medications were originally developed for treating allergies but found to cause a Parkinson's disease-like tremor response in patients. Scientists knew that Parkinson's patients had abnormally low dopamine levels, which caused their shaking. This relationship between symptoms suggested that symptoms of schizophrenia were related to excess dopamine.
-Ex: people with Parkinson's develop schizophrenic symptoms if they take too much L-dopa, a medication that raises dopamine levels.
-Ex: people who take high doses of amphetamines, which increase dopamine activity in the brain, may develop amphetamine psychosis - a syndrome similar to schizophrenia.

Researchers have located the dopamine receptors to which antipsychotic drugs bind - the drugs are apparently dopamine antagonists that bind to receptors, preventing dopamine from binding and the neuron from firing. This suggests that in schizophrenia, the messages travelling from dopamine-sending neurons to dopamine-receptors (D-2) may be transmitted to easily or too often. An appealing theory because certain dopamine receptors are known to play a key role in guiding attention.

Research since the 60s supports and clarifies this hypothesis.