The Pathogenesis Of Schizophrenia

Kraepelin first introduced the idea that abnormalities in neurodevelopment are related to the pathogenesis of schizophrenia (Lewis, 1989). This hypothesis was presented by D.R. Weinberger in 1987 but only focused on pathogenesis and failed to address etiology (Weinberger, 1989). This hypothesis was based on observations using modern imaging techniques that revealed some structural brain changes at the onset of illness focusing on the concept of a “lesion” (Turner et al., 1986). Schizophrenia research has been influenced greatly by this hypothesis in the past fourteen years and has contributed to the reestablishment of schizophrenia as a brain disease. In addition to this, longstanding clinical observations of premorbid features that are
Harvey et al., (1999) and Fucetola et al., (2000) add to this debate in suggesting that schizophrenia is not just simply a classic neurodegenerative disorder although there is some evidence that some neurodegeneration may contribute to the pathogenesis of schizophrenia (Woods, 1998; Lieberman,
As mentioned previously, researchers have agreed on a familial vulnerability to schizophrenia despite the genes associated with the disorder being elusive. Although researchers have investigated the idea of differential rates of the disorder among sociocultural groups, the casual role of the environment is still questioned. Research has revealed that social environment can play a role in the onset of psychotic disorders (van Os & McGuffin, 2003). Furthermore, findings from general and genetic epidemiology show that the relationship between genotype and phenotype, in the case of psychosis, is mediated by the environment. This gene-environment interaction is agreed upon between most geneticists in the case of schizophrenia. Literature conducted on the genetic association with schizophrenia such as genetic heritability modelling procedures and molecular genetics typically ignore this interaction. As a result of this, van Os & McGuffin (2003) concluded that there is an underestimation of the role of the social environment in the etiology of schizophrenia. Furthermore, as researchers have ignored the role of the environment, genes conferring risk have not been identified resulting in a gap in schizophrenic