biological explanations

• Genetic basis

  Family studies Candidate genes
• Neural correlates

  Original dopamine hypothesis Revised dopamine hypothesis
• Family studies have show that the risk of SZ increases in line with genetic similarity to someone with SZ.

  Gottesman (1991) conducted a large-scale family study and found much higher concordance rates in MZ twins (48%) in comparison to DZ twins (17%), suggesting a genetic explanation.
• If we know genetics have a role, the logical thing to do would be to identify the candidate genes responsible.

  SZ appears to be polygenic, meaning a number of different genes are involved in the development of SZ (around 108 genes in fact!)
• weakness

  There is clear evidence to show that environmental factors also increase the risk of SZ e.g family and cognitive dysfunction. The fact that concordance rate in MZ twins who share all of their genes was not 100% suggests other factors must play a role. Genetic factors alone cannot provide a complete explanation for SZ.
• Neural correlates

  Brain structure or function related to the cause of Schizophrenia. The best known neural correlate of SZ is the neurotransmitter dopamine.
• Original dopamine hyp

  SZ is caused by high levels of dopamine (hyperdopaminergia) in subcortical areas of the brain. e.g. an excess of DA in pathways from the subcortex to Boca's area may explain speech poverty.
• updated dopamine hyp

  SZ is caused by low levels of dopamine (hypodopaminergia) in cortex areas of the brain. e.g. low DA in the prefrontal cortex could explain cognitive problems
• one strength of the biological explanation for sz is research spport. There is now strong evidence for genetic vulnerability to schizophrenia from a variety of sources. E.g. Gottesman’s (1991) study. Additionally, Tienari et al.’s (2004) adoption study found that children of schizophrenia sufferers are still at heightened risk of schizophrenia if adopted into families with no history of schizophrenia. therefore there is a lot of evidence for sz being passed through genetics as well as research improving validity
• one strength of the biological explanation for schizophrenia is that dopamine plays a role. Much of the evidence supporting the dopamine hypothesis comes from drug treatments which change the levels of dopamine activity in the brain. Dopamine agonists which increase dopamine levels have been found to make schizophrenia worse. Antipsychotic drugs which decrease dopamine levels, however, reduce the symptoms of schizophrenia. this supports the origional dopamine hypothesis as it suggests sz is caused by high dopamine levels
• one weakness of the biological explanation of sz is contradictory research. Noll (2009) argues that antipsychotic drugs do not alleviate hallucinations and delusions in about 1/3 of people experiencing these symptoms. Also, in some people, hallucinations and delusions are present despite levels of dopamine being normal. this suggests dopamine levels are not linked to sz symptoms as people with normal dopamine levels show symptoms.
• one weakness of the biological explanation of sz is we can not determine cause and effect. Although studies of neural correlates are useful in flagging up particular brain systems that may not be working properly, this kind of evidence does not prove that the activity in the brain region causes the symptom. this means that we can not determine wheather neural correlates cause sz or a symptom of sz, reducing the validity of the explanation.