AQA A-level Psychology: Revision Made Easy - Jean-Marc Lawton 2017
Biological explanations for schizophrenia
Biological explanations see schizophrenia as physiologically determined. The genetic explanation sees the disorder as transmitted through hereditary means. It is not thought that there is a single ’schizophrenia gene’ but instead that several genes are involved — the more of these genes an individual has, the more vulnerable they are to developing schizophrenia, though an environmental trigger would also be needed for the onset of the condition. The dopamine hypothesis sees the development of schizophrenia as being related to abnormal levels of the hormone and neurotransmitter dopamine. High levels of dopamine in the mesolimbic dopamine system are associated with positive symptoms, while high levels in the mesocortical dopamine system are associated with negative symptoms. It is probable that genetic factors are linked to faulty dopaminergic systems in sufferers of the condition. The idea of neural correlates is that abnormalities within specific brain areas may be associated with the development of schizophrenia. Scanning has found enlarged ventricles in central brain areas and the prefrontal cortex, especially in those suffering negative symptoms. Abnormalities have also been found in the Wernicke brain area, which with its role in language abilities may explain the difficulties many schizophrenics have in producing coherent speech.
Fig 12.2 Several genes are suspected of being involved in the development of schizophrenia
Avramopoulos et al. (2013) assessed the contribution of genetics to the development of schizophrenia. They sequenced genes associated with the neuregulin signalling pathway, which relays signals within the nervous system. The researchers found that some families with high levels of schizophrenia had multiple neuregulin signalling-related gene variants while others had none. Schizophrenics with neuregulin signalling gene variants experienced more hallucinations but had less impairment than the other schizophrenia patients. The findings therefore suggest that individually harmless genetic variations, which affect related biochemical processes, may unite to increase vulnerability to schizophrenia, but additionally provide support for the idea that schizophrenia is not a single disorder at all but is actually a group of related disorders. Patients without neuregulin signalling-related variants have variants in a different pathway and therefore different symptoms.
• Gottesman & Shields (1976) reviewed 5 twin studies and reported a concordance rate of between 75 per cent and 91 per cent for MZ (identical) twins with severe forms of schizophrenia, suggesting that genetics plays a larger role with chronic forms of the disorder. Torrey et al. (1994), reviewing evidence from twin studies, found that if 1 MZ twin develops schizophrenia, there is a 28 per cent chance that the other twin will too, again supporting the idea that schizophrenia is inherited.
• Kessler et al. (2003) used PET and MRI scans to compare people with schizophrenia with non-sufferers, finding that the schizophrenics had elevated dopamine receptor levels in the basal forebrain and substantia nigra/ventral tegemental brain areas. Differences in cortical dopamine levels were also found, suggesting that dopamine is important in the onset of schizophrenia.
• Tilo (2001) used fMRI scans to find that severity of thought disorder, a core symptom of schizophrenia, was negatively correlated with activity in the Wernicke brain area, associated with producing coherent speech. This suggests specific brain areas are linked to schizophrenia.
Adoption studies show that adopted children with a high genetic risk of developing schizophrenia (as there was a high incidence of the disorder among biological relatives) are more sensitive to non-healthy rearing practices by adopted families, illustrating how genetic and environmental factors interact in the development of schizophrenia.
Several neurotransmitters, not just dopamine, may be involved in the development of schizophrenia. More newly developed anti-schizophrenia drugs suggest that glutamate and serotonin also have an influence.
Some patients may not respond to treatment as structural brain damage does not permit anti-psychotic drugs to have an effect in reducing symptom levels.
Although twin studies suggest a genetic component to the development of schizophrenia, they do not consider the influence of social class and socio-psychological factors between twins, nor do they consider shared environmental influences, which lowers the validity of the evidence for the genetic explanation.
Differences in the biochemistry of schizophrenics, such as with dopamine levels, may be an effect of being schizophrenic rather than a cause.
Some non-schizophrenics have enlarged ventricles in brain tissue, but not all schizophrenics do, which refutes the idea of schizophrenia being linked to loss of brain tissue. It may be that loss of brain tissue is a result of schizophrenia rather than a cause.
The main practical application of biological explanations is in drug therapies. Anti-schizophrenic drugs, such as phenothiazines, work by decreasing dopamine activity, with the effectiveness of such drugs giving support to the dopamine hypothesis.