Biological Explanations

• there are genetic explanations that suggest that there are several genes involved in increasing an individual's vulnerability to schizophrenia through hereditary means
• twin studies: identical twins share 100% of their DNA whereas non-identical twins share around 50%. if schizophrenia is caused by genetics then concordance rates will be higher among identical twins than non-identical twins
• adoption studies: adopted children whose biological parents were diagnosed with schizophrenia are more likely to develop the disorder themselves compared to adoptees where neither parent has schizophrenia
• Varma and Sharma (1993) found a concordance rate of 35% for first degree relatives of individuals with schizophrenia, compared to 9% in first degree relatives of non-schizophrenics. this indicates a role in genetic factors
• Parmas et al (1993) conducted a longitudinal family study of schizophrenia, finding that 16% of children whose mothers had schizophrenia also developed the disorder, compared with 2% of the children whose mothers didn't have the disorder. this also suggests a link to genetics
• the dopamine hypothesis claims that excessive amounts of dopamine or an oversensitivity of the brain to dopamine is the cause of schizophrenia. it also states that messages from neurons that transmit dopamine fire too easily or too often, leading to the symptoms of schizophrenia
• Snyder (1976) argued that if too much dopamine is realised during synapse it can lead on the onset of schizophrenia
• most antipsychotic drugs tend to block the activity of dopamine in the brain. they do this by reducing the activity in the neural pathways in the brain that use dopamine as a neurotransmitter. this strengthens the case of dopamine in schizophrenia
• Iversen (1979) found that in post-mortems on people who had schizophrenia, an excessive amount of dopamine was found in the limbic system. this suggests that the neurotransmitter is involved in the disorder
• Patel et al (2010)used PET scans to assess the dopamine levels in schizophrenia and non schizophrenia individuals and found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls
• Davis and Kahn (1991) proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain. particularly the mesolimbic.
• Davis and Kahn (1991) also proposed that the negative and cognitive symptoms of schizophrenia are through to arise from a deficit of dopamine in areas of the brain of the prefrontal cortex. the mesocortical pathway.
• Leucht et al (2013) carried out a meta analysis of 212 studies that analysed the effectiveness of different antipsychotic drugs compared with a placebo. they found that all the drugs were significantly more effective than placebos in treatment of positive and negative symptoms. this suggests that drug treatments are important for treating the disorder
• Noll (2009) argued that antipsychotic drugs don't alleviate hallucinations and delusions in around 1/3 of people experiencing the symptoms. this shows how drug treatments aren't always effective
• several studies have shown changes in the hippocampus in schizophrenia patients. there are failings in the nerve connections between the hippocampus and the prefrontal cortex and these have been found to be related with the degree of working memory impairments
• the prefrontal cortex is involved in executive control. Weinberger and Gallhofer (1997) argue that research suggests that this area of the brain is impaired for people who have schizophrenia
• the ventral striatum is thought to be involved in the development of avolition. Juckel et al (2006) have measured activity of activity in the ventral striatum in schizophrenia and found lower levels of activity then those observed in control groups