BIO EXP

• What does the biological explanation of schizophrenia suggest?

  • Emphasises the role of inherited factors and dysfunction of brain activity
• How are candidate genes linked to schizophrenia? (genetic exp)

  • Individual genes are associated with risk of inheritance
  • Schizophrenia is polygenic (requires a number of genes to work in combination)
  • Also aetiologically heterogeneous
• Research support for candidate genes and schizophrenia having a genetic basis

  • Gottesman 1991- family study
  • Stephen Ripke et al (2014)- genome-wide study
• What is the dopamine hypothesis?

  • An example of a neural correlate
  • Dopamine is believed to be involved in the symptoms of schizophrenia
• Dopamine hypothesis: Hyperdopaminergia

  • High levels/activity of dopamine in the SUBCORTEX (central areas of the brain)
  • E.g. an excess of dopamine receptors in Broca's area may be associated with speech poverty and auditory hallucinations
• Dopamine hypothesis: Hypodopaminergia

  • Abnormal dopamine systems in the brain's prefrontal cortex (responsible for thinking and decision making)
  • GOLDMAN-RAKIC ET AL identified this
• What is a neural correlate of a negative symptom? (bio exp.)

  • The development of avolition may involve the abnormality of the ventral striatum
  • Supported by JUKEL ET AL, found negative correlation between activity on ventral striatum and severity of negative symptoms
• What is a neural correlate?

  A measurement of the structure/function of the brain that correlates with an experience.
• What is a neural correlate of a positive symptoms?

  • Compared auditory hallucination group to control
  • ALLEN ET AL found lower activation levels in the superior temporal gyrus and anterior cingulate gyrus in hallucination group
• Research support for gene influence in schizophrenia?

  • STEPHEN RIPKE found 108 genetic variations associated with an increased risk of schizophrenia
  • The genes included a number of neurotransmitters including dopamine which may contribute to suggesting there are biological influences
• Gottesman's family study- support for genetic influence (AO3)

  • large scale family study assessing the percentage risk of developing schizophrenia within each family relation (e.g. parents, siblings, twins etc.)
  • identical twins have a 48% concordance rate of developing schizophrenia with 100% of their genes being shared
  • (fraternal 17% which share 50% of genes remphasising this)
  • supports the idea that genes have a large influence on inheritance and concordance rates
  • The more closely related, the higher the risk, therefore schizophrenia does have a genetic influence.
• What is a limitation for neural correlates?

  • Correlations found does not mean a causation/cause and effect relationship has been established
  • Cannot decipher whether the abnormal activity in the region causes the symptom or vice versa
  • Juckel's ventral striatum finding may be the result of negative symptoms impacting the amount of information passing through the striatum resulting in less activity
  • Therefore, unable to tell us much about SZ symptoms and correlates
• What is a limitation of the dopamine hypothesis?


  • Not a complete explanation for SZ
  • Genes identified by Ripke code for the production of other neurotransmitters
  • Therefore may suggest dopamine is likely to be a factor, other neurotransmitters may also be involved
  • Glutamate has had more focus within research due to its possible role in symptoms and vulnerability
  • Therefore dopamine hypothesis cannot account as a whole explanation, limiting its ability
• Strength/support for dopamine hypothesis

  • Sources to support dopamine as a factor in SZ vulnerability
  • Curran et al -> dopamine agnoists (e.g. amphetamines) can increase levels and therefore produce SZ-like symptoms in people who are not diagnosed with it
  • Tauscher et al-> Antipsychotic drugs work by reducing dopamine activity to reduce symptoms
  • Lindstroem et al -> chemicals needed to produce dopamine are taken up faster in brains of people with SZ, suggesting they produce more and have faster uptake
• Strength/support for genetic explanations for SZ

  • Gottseman family wide study, genetic similarity and shared risk of SZ are closely related
  • Tienari et al -> adoption study found that children of people with SZ are at heightened risk even if adopted into a family with no history of SZ
  • Ripke et al -> found 108 candidate genes that show an increased vulnerability to developing SZ, a molecular level study supporting the genetic basis