Biological explanation of Schizophrenia

• What are the definitions of key words related to biological explanations of schizophrenia?

  • Biological explanations: emphasis on the role of inherited factors and dysfunction of brain activity in the development of a behaviour/mental disorder
  • Dopamine hypothesis: claims that excess of dopamine ( a neurotransmitter) = associated with positive symptoms of schizophrenia
  • Genetics: inherited factors make certain individuals more likely to develop a behaviour/metal disorder
  • Neural correlates: changes in neuronal events + mechanisms that -> characteristic symptoms of a behaviour/mental disorder
• What did family studies show about schizophrenia? Who's study provided evidence?

  • risk of schizophrenia increases in line with genetic similarity
  • the closer the degree of genetic relatedness, the greater the risk
  • Gottesman (1991) : the more closely related a person is to someone with schizophrenia, the greater the risk they have of developing it too.
  • Children with 2 schizophrenic parents = concordance rate of 46%
  • Children with 1 schizophrenic parent = concordance rate of 13%
  • siblings had a concordance rate 9%
  • HOWEVER may have been due to environmental similarities
• What did twin studies suggest about schizophrenia? Whose study provided evidence of the genetic links?

  • if monozygotic twins (identical) are more concordant than dizygotic twins (fraternal) then it suggests greater similarity is due to genetic factors
  • Joseph (2004)
  • MZ twins = 40.4%
  • DZ twins = 7.4%
• What did research into candidate genes show about schizophrenia?

  • revealed that 1 single gene alone did not cause schizophrenia. It is polygenic
  • Genes most likely involved are those coding for neurotransmitters like dopamine
  • Ripke et al (2014) combined data from studies: found 108 separate genetic combinations were associated with slightly increased risk of schizophrenia
  • discovered that schizophrenia is aetiologically heterogeneous - meaning different combinations of factors including genetic variation can -> condition.
• What did adoption studies show about schizophrenia?

  • use adoption studies as a way to separate genetic and environmental influences, since comparisons can be made between adopted children and biological mothers (separate environments)
  • Tienari et al. (2000) Finland study of 164 adoptees whose biological mother = schizophrenic
  • 11 (6.7%) also schizophrenic, but only 4/197 (2%) of the control group had schizophrenia without a schizophrenic mother.
  • Conclusion : confirmed genetic links to schizophrenia.
• What did research into neural correlates show about schizophrenia?

  • research focused on the important role of neurotransmitter dopamine + on areas of the brain influential in onset/development of schizophrenia
  • dopamine hypothesis + specific areas of brain (e.g prefrontal cortex, hippocampus, grey + white matter) are all relevant in development of schizophrenia
• What is the dopamine hypothesis + research related to it?

  • claims excess of neurotransmitter dopamine = associated with pos. symptoms of schizophrenia
  • schizophrenics have high numbers of D2 receptors on receiving neurons -> more dopamine binding + more neurons firing
• Describe the effect of drugs on dopamine (schizophrenia)

  • Amphetamine = dopamine agonist (stimulates nerve cells containing dopamine)
  • 'normal' individuales exposed to large doses of dopamine agonist drugs can develop characteristic symptoms of a schizophrenic episode (disappears in absence of drug)
  • Dopamine antagonists reduce positive symptoms
  • block activity of dopamine in brain, by reducing activity in neural pathways that use dopamine
• What has research into the dopamine hypothesis found?

  • Davis and Khan (1991) : Pos. symptoms = excess of dopamine in subcortical areas (particularly mesolimbic pathway). Neg. symptoms = deficit of dopamine in subcortical areas of the prefrontal cortex (mesocortical pathway)
  • Patel et al (2010) found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to normal controls.
• What areas of the brain are associated with schizophrenia?

  prefrontal cortex, the hippocampus, grey matter, white matter
• How is the prefrontal cortex associated with schizophrenia?

  • involved in executive control (planning, reasoning, judgement)
  • Weinberger + Gallhofer (1997) research shows area was impaired in patients with schizophrenia
  • Hypothesized that cognitive symptoms of schizophrenia = due to deficits in PFC + its connections to other areas (particularly the hippocampus)
• How is the hippocampus associated with schizophrenia?

  • area in temporal lobe
  • Conrad et al. (1991) anatomical changes in hippocampus in schizophrenia patients
  • Mukai et al. (2015) deficits in nerve connections between this + PFC correlates to memory impairments
  • Goto + Grace (2008) suggest hippocampal dysfunction may influence levels of dopamine release in basal ganglia - indirectly affect processing in PFC.
• How is grey matter associated with schizophrenia?

  • reduced volume in temporal + frontal lobes in patients with schizophrenia
  • Hartberg et al. (2011) Enlarged ventricles - consequence of nearby parts of the brain not developing properly/damaged -> particularly associated with neg. symptoms
  • Cannon et al. (2014) found that individuals with high risk of schizophrenia = steeper rate of grey matter loss + greater rate of expansion of brain ventricles
• How is white matter associated with schizophrenia?

  • in brain cord + spinal area + made up of nerve fibers covered in myelin which helps conduct info quickly through CNS = efficient info processing.
  • Du et al. (2013) reduced myelination of white matter pathways in schizophrenia patients (particularly in pathway between PFC + hippocampus)
• What are the key points of evaluation of the biological explaination of schizophrenia?

  Strength : There is evidence supporting the dopamine hypothesis, through evidence of successful drug treatment.

  Strength : Understanding of genetic influence on development of schizophrenia has allowed the development of genetic counselling

  Limitation : Adoption studies assume that adoptive parents who adopt children with schizophrenia are no different to adoptive parent with adoptive children with normal backgrounds

  Limitation : Twins studies actually fail to eliminate environmental factors.
• Strength of biological explanations (schizophrenia) : Evidence supporting dopamine hypothesis

  • Leucht et al (2013) meta-analysis
  • concluded that anti-psychotic drugs tested were significantly more effective than a placebo
  • achieved by reducing dopamine levels which the dopamine hypothesis claims is what causes schizophrenia.
  • Furthermore suggests early intervention might prevent development of later stages of disorder.
  • Addington et al (2015) used dif. methods to predict who will develop psychoses such as schizophrenia
  • Therefore better understands how schizophrenia develops .
• Strength of biological explanations (schizophrenia) : understanding genetic influence has led to genetic counseling

  • if 1+ parents have a relative w/schizophrenia, they risk having a child who would develop the condition
  • based on Gottesman's study - 2% probability if aunt/uncle has schizophrenia, 6% probability if half-sibling has it.
  • genetic counseling allows parents to make informed decisions about whether to have children who risk developing schizophrenia.
  • HOWEVER risk is only an average figure based on risk across the whole population. Role of the environment too.
• Limitation of biological explanations (schizophrenia) : Adoption studies make poor assumptions

  • is an assumption that adoptees are non 'selectively placed' + that adoptive parents who adopt child with schizophrenic parent are no different to those adopting child w/ 'normal' background.
  • Heston (1966) assumed children of anyone in mental hospital would = inherited tendency to 'feeble-mindedness, insanity and degeneracy'
  • Joseph (2004) unlikely that children w/schizophrenic mothers would be placed into same type of adoptive families as children with normal background. (selectively placed)
• Limitation of biological explanations (schizophrenia) : Twin studies fail to eliminate environmental factors

  • crucial assumption of twin studies is that environments of MZ (monozygotic/identical) + DZ (dizygotic/fraternal) twins would be the same
  • Joseph (2004) points out how MZ twins = more similarly treated + encounter more similar environments in comparison to DZ twins
  • MZ = likely to experience more 'identity confusion'
  • Suggests differences in concordance rates between MZ +DZ twins is not due to only genetics, may still be influenced by environment.