Investigations into the etiology of schizophrenia have focused mainly on two areas:
It is well known that the risk of schizophrenia increases when there is a history of this disease in the family and that this risk is greater in increasing the degree of genetic affinity with the affected family member. However, this supposed genetic basis of schizophrenia was questioned until the late 60s, arguing that the family factor could be due to the dynamics and own interactions of the affected families.
Adoption studies examined the risk of schizophrenia in adopted children of parents with the disease, demonstrating that this risk is associated with the presence of schizophrenia in one of the biological parents and not the presence of the disease in the adoptive parents. Twin studies, which showed a concordance three times higher among identical twins (up to 40%) than among fraternal twins (between 10 and 15%). Studies of familial risk, which showed a risk of 7% in the general population, compared with a risk of 10 to 15% by siblings or children of a person with schizophrenia, the risk increases to 40% if both parents having the disease.
Additionally, it was determined that genetic factors may contribute to 80% by variability between individuals affected phenotype. These data led to the search for genetic variants that were associated with the disease and allow understand the biological processes that are affected in the brains of patients with schizophrenia. Through the search for single nucleotide...
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...that consumption in patients with a first psychotic episode is greater than found in the general population. Other population epidemiological studies have shown that teens who use marijuana weekly, show an increased risk of developing acute psychosis 3 or more years later, compared to teens who do not use marijuana.
In recent years, thanks to the development of histopathological techniques and neuro image (eg. Magnetic resonance imaging Fig.1, positron emission tomography Fig.2), have managed to detect abnormalities in certain brain structures and alterations in brain functioning of people with schizophrenia. These findings would support the theory of neuro abnormal development that postulates the existence of alterations in the normal formation of synapses and neuronal migration during brain formation and its connections (neurodevelopmental encephalopathy).
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