2. Biological Explanations

• The genetic basis - candidate genes

  • Schizophrenia is polygenic as there are a number of genes involved
  • Dopamine is most likely involved and codes for neurotransmitters
  • Ripke et al. study - combined all previous data from a genome wide study of Sz. 37,000 people with a diagnosis, 113,000 controls and 108 genetic variations associated
  • Sz is aetiologically heterogenous
• The genetic basis - the role of mutation

  • Sz can have a genetic origin in the absence of a family history of the disorder
  • Radiation or viral infection
  • Evidence for mutation comes from positive correlations between paternal age and risk of Sz
• Neural correlates - the original dopamine hypothesis

  • Neural correlates are levels of activity in the brain that occur in conjunction with schizophrenia.
  • The Dopamine Hypothesis focuses on the action of DA in the brain
  • The original hypothesis theorised that heightened levels of DA (hyperdopaminergia) in subcortical regions of the brain could explain symptoms
  • Areas which link to Broca’s area are thought to be responsible for language deficits such as poverty of speech and/or auditory hallucinations
• Neural correlates - the updated dopamine hypothesis

  • The updated hypothesis argues that hypodopaminergia (lowered levels of DA) can explain Sz symptoms
  • Hypodopaminergia in the prefrontal cortex are thought to cause cognitive deficits such as avolition and poor focus
  • This can account for the negative symptoms of Sz
• AO3 for the genetic basis - research support

  • Hilker et al. - showed a concordance rate of 33% for MZ twins and 7% for DZ twins, indicating that the more genetically similar the twins are the higher the concordance rate, supporting the role of genetics in the development of Sz
  • COUNTERPOINT - environmental factors are held constant because twins are brought up together and must therefore experience similar environment.