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Wikipedia:

Causes:
• Schizophrenia is likely to be a diagnosis of complex inheritance.
• Several genes interact to generate risk for schizophrenia .

Genetic:
• Current research suggests that environmental factors play a significant role in the
expression of any genetic disposition towards schizophrenia.
• Recent twin studies suggested a more than 28% chance of one identical twin
obtaining the diagnosis if the other already has it, but such studies does not take
into account similarities of social class and socio-psychological factors between
the twins.
• A 2003 review of linkage studies listed seven genes as likely to increase risk for a
later diagnosis of the disorder. Two more recent reviews have suggested that the
evidence is currently strongest for two genes known as dysbindin (DTNBP1) and
neuregulin (NRG1).

Environmental:
• Considerable evidence indicates that stressful events cause/trigger schizophrenia.

Perinatal brain development:


• It is thought that causal factors in early neurodevelopment including during
pregnancy can increase risk of developing schizophrenia later.
• Some researchers postulate that the correlation is due to viral infections during the
third trimester (4-6 months) of pregnancy.
• There is now significant evidence that prenatal exposure to infections increases
the risk for developing schizophrenia later in life.

Childhood and adolescent development:

Adult brain structure:


• Differences in the size and structure of certain brain areas have been found in
some adults diagnosed with schizophrenia.
• Discovery of ventricular enlargement in people diagnosed with schizophrenia
with negative symptoms most prominent.

Neuropsychology and brain function:


• Neuropsychological tests and brain imaging technologies such as fMRI and PET
to examine functional differences in brain activity have shown that differences
seem to most commonly occur in the frontal lobes, hippocampus and temporal
lobes.
• These differences are heavily linked to neurocognitive deficits which often occur
with schizophrenia, particularly in areas of memory, attention, problem solving,
executive function and social cognition.

Neurochemical pathways:
• dopamine hypothesis of schizophrenia
• overly simplistic as a complete explanation because atypical antipsychotic
medication can be equally effective as typical antipsychotic medication but also
affects serotonin function and less dopamine blocking effect.
• In addition dopamine pathway dysfunction has not been reliably shown to
correlate with symptom onset or severity.
• Interest has also focused on glutamate and reduced function of NMDA in
schizophrenia.
• Suggested by abnormally low levels of glutamate receptors found in post-mortem
brains of people diagnosed with schizophrenia. Discovery that glutamate blocking
drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive
problems associated with the condition. Fact that reduced glutamate function is
linked to poor performance on tests requiring frontal lobe and hippocampal
function and that glutamate can affect dopamine function suggest an important
mediating and possibly causal role of glutamate pathways in schizophrenia.
Further support come from preliminary trials suggesting the efficacy of coagonists
at the NMDA receptor complex in reducing some of the positive schizophrenic
symptoms.

Psychosocial factors:
see article

Autoimmune theory:
• Growing evidence of autoimmunity in etiology and pathogenesis of schizophrenia

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