biological explanation

• genetic basis

  • runs in families
  • strong relationship between degree of genetic similarity and shared risk of sz
  • mz twins = 48% and dz twins = 17%
  • candidate genes are individual genes that increase the risk of developing sz
  • polygenic = combination of genes can give a risk
  • aetiologically heterogenous = different combinations of factors can give a risk
  • 108 genetic variations associated with sz e.g genes that code for dopamine
• dopamine hypothesis

  • neurotransmitters work differently in someone with sz, particularly dopamine
  • hyperdopaminergia in the subcortex = high levels of dopamine in the subcortex e.g excess in brocas causes speech poverty
  • hypodopaminergia in the cortex = low levels of dopamine in the prefrontal cortex can cause negative symptoms
• neural correlates

  • negative symptoms = abnormality of ventral straitum involved with avolition
  • positive symptoms = lower activation levels in superior temporal gyrus and anterior cingulate gyrus can cause hallucinations
• strength

  • adoption studies show that children of people with sz are still at heightened risk even if adopted by families with no sz history
  • very strong evidence for genetic vulnerability
  • genetic susceptibility needed along with other environmental factors
• mixed evidence for dopamine hypothesis

  • dopamine agonists increase dopamine and give people sz symptoms even though they dont have sz
  • antipsychotic drugs reduce dopamine activity
  • both suggest important role for dopamine
  • dopamine doesnt provide a full explanation as some candidate genes code for other neurotransmitters not just dopamine
  • may be down to a neurotransmitter called glutamate
• role of mutation

  • mutation in parental dna by viral infection can give a risk when theres an absence of family history
  • positive correlation between paternal age (causes the mutation) and developing sz
  • 0.7% in fathers under 25 and 2% in fathers over 50