Several factors may contribute to Schizophrenia, including:
 

Genes, because the illness runs in families The environment, such as viruses and nutrition problems before birth Different brain structure and brain chemistry.

Scientists have learned a lot about Schizophrenia. They are identifying genes and parts of the brain that may play a role in the illness. Some experts think the illness begins before birth but doesn't show up until years later. With more study, researchers may be able to predict who will develop Schizophrenia.

Some Details
Experts think Schizophrenia is caused by several factors.

Genes and Environment. Scientists have long known that Schizophrenia runs in families. The illness occurs in 1 percent of the general population, but it occurs in 10 percent of people who have a first-degree relative with the disorder, such as a parent, brother, or sister. People who have second-degree relatives (aunts, uncles, grandparents, or cousins) with the disease also develop Schizophrenia more often than the general population. The risk is highest for an identical twin of a person with Schizophrenia. He or she has a 40 to 65 percent chance of developing the disorder.
We inherit our genes from both parents. Scientists believe several genes are associated with an increased risk of Schizophrenia, but that no gene causes the disease by itself. In fact, recent research has found that people with Schizophrenia tend to have higher rates of rare genetic mutations. These genetic differences involve hundreds of different genes and probably disrupt brain development.

Other recent studies suggest that Schizophrenia may result in part when a certain gene that is key to making important brain chemicals malfunctions. This problem may affect the part of the brain involved in developing higher functioning skills. Research into this gene is ongoing, so it is not yet possible to use the genetic information to predict who will develop the disease.
Despite this, tests that scan a person's genes can be bought without a prescription or a health professional's advice. Ads for the tests suggest that with a saliva sample, a company can determine if a client is at risk for developing specific diseases, including Schizophrenia. However, scientists don't yet know all of the gene variations that contribute to Schizophrenia. Those that are known raise the risk only by very small amounts. Therefore, these "genome scans" are unlikely to provide a complete picture of a person's risk for developing a mental disorder like Schizophrenia.
In addition, it probably takes more than genes to cause the disorder. Scientists think interactions between genes and the environment are necessary for Schizophrenia to develop. Many environmental factors may be involved, such as exposure to viruses or malnutrition before birth, problems during birth, and other not yet known psychosocial factors.

Different Brain Chemistry and Structure. Scientists think that an imbalance in the complex, interrelated chemical reactions of the brain involving the neurotransmitters dopamine and glutamate, and possibly others, plays a role in Schizophrenia. Neurotransmitters are substances that allow brain cells to communicate with each other. Scientists are learning more about brain chemistry and its link to Schizophrenia.
Also, in small ways the brains of people with Schizophrenia look different than those of healthy people. For example, fluid-filled cavities at the center of the brain, called ventricles, are larger in some people with Schizophrenia. The brains of people with the illness also tend to have less gray matter, and some areas of the brain may have less or more activity.

Studies of brain tissue after death also have revealed differences in the brains of people with Schizophrenia. Scientists found small changes in the distribution or characteristics of brain cells that likely occurred before birth. Some experts think problems during brain development before birth may lead to faulty connections. The problem may not show up in a person until puberty. The brain undergoes major changes during puberty, and these changes could trigger psychotic symptoms. Scientists have learned a lot about Schizophrenia, but more research is needed to help explain how it develops.
A Combination of Genetic and Environmental Factors play a role in the development of Schizophrenia. People with a family history of Schizophrenia who have a transient psychosis have a 20–40% chance of being diagnosed one year later.

Genetic
Estimates of heritability vary because of the difficulty in separating the effects of genetics and the environment. The greatest risk for developing Schizophrenia is having a first-degree relative with the disease (risk is 6.5%); more than 40% of monozygotic twins of those with Schizophrenia are also affected. It is likely that many genes are involved, each of small effect and unknown transmission and expression. Many possible candidates have been proposed, including specific copy number variations, NOTCH4, and histone protein loci. A number of genome-wide associations such as zinc finger protein 804A have also been linked. There appears to be significant overlap in the genetics of Schizophrenia and bipolar disorder. Evidence is emerging that the genetic architecture of Schizophrenia involved both common and rare risk variation.
Assuming a hereditary basis, one question from evolutionary psychology is why genes that increase the likelihood of psychosis evolved, assuming the condition would have been maladaptive from an evolutionary point of view. One idea is that genes are involved in the evolution of language and human nature, but to date such ideas remains little more than hypothetical in nature.

Environment
Environmental factors associated with the development of Schizophrenia include the living environment, drug use and prenatal stressors. Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of Schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.

Drug use
Amphetamine, cocaine, and to a lesser extent alcohol, can result in psychosis that presents very similarly to Schizophrenia. Although it is not generally believed to be a cause of the illness, people with Schizophrenia use nicotine at much greater rates than the general population. About half of those with Schizophrenia use drugs or alcohol excessively. Evidence supports a link between earlier onset of psychotic illness and cannabis use; alcohol use is not associated with an earlier onset of psychosis. Other drugs may be used only as coping mechanisms by individuals who have Schizophrenia to deal with depression, anxiety, boredom, and loneliness. There is evidence that alcohol abuse via a kindling mechanism can occasionally cause the development of a chronic substance induced psychotic disorder, i.e. Schizophrenia. The more often cannabis is used; the more likely a person is to develop a psychotic illness, with frequent use being correlated with twice the risk of psychosis and Schizophrenia. Whether cannabis use is a contributory cause of Schizophrenia, rather than a behavior that is simply associated with it, remains controversial.

Developmental Factors
Factors such as hypoxia and infection, or stress and malnutrition in the mother during fetal development, may result in a slight increase in the risk of Schizophrenia later in life. People diagnosed with Schizophrenia are more likely to have been born in winter or spring (at least in the northern hemisphere), which may be a result of increased rates of viral exposures in utero. The increased risk is about 5 to 8%.
 
Mechanisms
A number of attempts have been made to explain the link between altered brain function and Schizophrenia. One of the most common is the dopamine hypothesis, which attributes psychosis to the mind's faulty interpretation of the misfiring of dopaminergic neurons.

Psychological
Many psychological mechanisms have been implicated in the development and maintenance of Schizophrenia. Cognitive biases have been identified in those with the diagnosis or those at risk, especially when under stress or in confusing situations. Some cognitive features may reflect global neurocognitive deficits such as memory loss, while others may be related to particular issues and experiences.
Despite a demonstrated appearance of blunted affect, recent findings indicate that many individuals diagnosed with Schizophrenia are emotionally responsive, particularly to stressful or negative stimuli, and that such sensitivity may cause vulnerability to symptoms or to the disorder. Some evidence suggests that the content of delusional beliefs and psychotic experiences can reflect emotional causes of the disorder, and that how a person interprets such experiences can influence symptomatology. The use of "safety behaviors" to avoid imagined threats may contribute to the chronicity of delusions. Further evidence for the role of psychological mechanisms comes from the effects of psychotherapies on symptoms of Schizophrenia.

Neurological
Functional magnetic resonance imaging (fMRI) and other brain imaging technologies allow for the study of differences in brain activity in people diagnosed with Schizophrenia. The image shows two levels of the brain, with areas that were more active in healthy controls than in Schizophrenia patients shown in orange, during an fMRI study of working memory.

Schizophrenia is associated with subtle differences in brain structures, found in 40 to 50% of cases, and in brain chemistry during acute psychotic states. Studies using 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. Reductions in brain volume, smaller than those found in Alzheimer's disease, have been reported in areas of the frontal cortex and temporal lobes. It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease. These differences have been linked to the neurocognitive deficits often associated with Schizophrenia. Because neural circuits are altered, it has alternatively been suggested that Schizophrenia should be thought of as a collection of neurodevelopmental disorders.

Particular attention has been paid to the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that phenothiazine drugs, which block dopamine function, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which trigger the release of dopamine, may exacerbate the psychotic symptoms in Schizophrenia. The influential dopamine hypothesis of Schizophrenia proposed that excessive activation of D2 receptors was the cause of (the positive symptoms of) Schizophrenia. Although postulated for about 20 years based on the D2 blockade effect common to all antipsychotics, it was not until the mid-1990s that PET and SPET imaging studies provided supporting evidence. The dopamine hypothesis is now thought to be simplistic, partly because newer antipsychotic medication (atypical antipsychotic medication) can be just as effective as older medication (typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in Schizophrenia, largely because of the abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with Schizophrenia, and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition. Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function, and glutamate can affect dopamine function, both of which have been implicated in Schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in the condition. But positive symptoms fail to respond to glutamatergic medication.