In genetic research, scientists found that a biological predisposition to schizophrenia could be inherited by some people who might develop this disorder later when they experience extreme stress, usually during late adolescence or early adulthood. Genetic Factors are often viewed on the basis of principles of the diathesis stress perspective. As Comer (2010) stated, the influence of genetic factors had been confirmed by “studies of (1) relatives of people with schizophrenia, (2) twins with this disorder, (3) people with schizophrenia who are adopted, and (4) genetic linkage and molecular biology” (p. 433).
According to Joober, Boksa, Benkelfat, and Rouleau (2002), researchers have found neither major genes that cause schizophrenia nor a gross neuropathological signature of schizophrenia. However, recent findings in genetic epidemiological research demonstrated additive and interactive genes could only place small effects from each but coherently manifest the genetic vulnerability for schizophrenia. To fully understand the genetics of schizophrenia, Joober et al. (2002) suggested further studies on the complex classic factors in relation to the inheritance of schizophrenia in non-mendelian mode and construction of “a phenotypic definition based on objective, reliable and reproducible measurements” (p. 343).
Taking advantage of salient progress in neuroscience in recent years, scientists have used neuroimaging to study the neurobiological processes that convey the mental disorder risk from the genes to the complex phenotypes. These studies resulted that “schizophrenia is highly heritable with a pattern consistent with both common and rare allelic variants and gene x environment interaction” (Hirvonen & Hietala, 2011, p. 89). In a study of schizophrenic genetics related to neurotransmitters, Hirvonen and Hietala (2011) revealed that people with a risk of schizophrenia share neurotransmitter abnormalities with changes in the dopamine system. Molecular imaging studies have shown that potential intermediate phenotypes that carry the risk for schizophrenia include increased striatal presynaptic synthesis, increased striatal D2 receptors, and increased cortical D1 receptors.
Comer, R. J. (2010). Abnormal psychology (8th ed.). New York, NY: Worth Publishers.
Hirvonen, J., & Hietala, J. (2011). Dysfunctional brain networks and genetic risk for schizophrenia: specific neurotransmitter systems. CNS Neuroscience & Therapeutics, 17(2), 89-96. doi:10.1111/j.1755-5949.2010.00223.x
Joober, R., Boksa, P., Benkelfat, C., & Rouleau, G. (2002). Genetics of schizophrenia: from animal models to clinical studies. Journal Of Psychiatry & Neuroscience, 27(5), 336-347.