Biological explanations of schizophrenia suggest that it is inherited and that there may be specific genes or neurological functions which predispose individuals to criminal behaviour.
Schizophrenia is seen as a poly genetic disorder as there is no direct causal gene, but several which are associated with a higher risk of developing the disorder, and we call these candidate genes. In 2004, salleh identified that neuregulin 1, dysbindin, and proline dehydrogenase increase the likelihood of the disorder as they affect the production and regulation of the neurotransmitters dopamine, serotonin and glutamate used in regulating mood.
Schizophrenia can also be resulted from mutations in parental DNA through factors like radiation, poison, or infection. This has stemmed from Brown et al in 2002 who showed a correlation with parental age (increased risk of mutation) and schizophrenia disorders.
gottesman - meta analysis of schizophrenics found a 48% concordance rates of 45% with monozygotic twins, 17% with dizygotic, and 1% with the general population
Tiernai found adopted children who's mothers suffered schizophrenia were more likely to develop the disorder than adopted children who's mothers did not.
Clinical and objective methods and meta analysis allows a large sample to be analysed increasing the generalisability and external validity of the results.
What are the weaknesss of genetic explanations for SZ
concordance rates are not 100% suggesting genetics can not provide a full comprehensive explanation for schizophrenia, additionally twins are usually brought up in similar environments therefore we cannot rule out external factors as an explanation on schizophrenia. This could be overcome by adoption studies however this would assume that children are not selectively placed and Joseph in 2004 found that prospective parents often receive information about the child prior to adoption, reducing the validity of the results.
Outline neural correlates as an explanation for SZ
Neural correlates i.e. brain structures and neurotransmitters have also been suggested as a cause for schizophrenia. An example of this is that research has shown that many people with schizophrenia have larger ventricles which contain brain fluid that maintains neuron function. This means they also have smaller brain volume elsewhere e.g. frontal cortex.
Another example of neural correlates as an explanation for schizophrenia is the dopamine hypothesis suggests that schizophrenia is caused when the neurons in the mesolimbic system are overactive due to an incresed level of dopamine, causing hallucinations and delusions. However researcher have now suggested that in the frontal cortex dopamine levels are too low causing under active neurons resulting in the negative symptoms of schizophrenia, so the model was revised.
Supporting evidence - torrey compared MRI brain images of those with and without schizophrenia and found that on average those with schizophrenia has ventricles around 15% larger.
Drug studies show that when SZ patients take drugs that reduce dopamine, their positive symptoms are reduced
Addington found that brain tissue in SZ can be predicted meaning early detecting and treatment is possible