biological explanations

• family studies -

  • confirmed risk of schizophrenia increases in line with genetic similarity to a relative with the disorder
  • Gottesman's (1991) large scale family study - 9% chance if individual is a sibling, 48% chance if they're an identical twin
  • family members share aspects of environment as well as many of their genes so correlation represents both
• candidate genes -

  • schizophrenia is polygenic - number of genes involves - most likely genes would be those coding for neurotransmitters including dopamine
  • Ripke et al (2014) combined all previous data from genome-wide studies of schizophrenia - genetic makeup of 37,000 people with diagnosis compared to 113,000 controls - 108 separate genetic variations were associated with slightly increased risk
  • its aetiologically heterozygous - different combination of factors including genetic variations can lead to the condition
• role of mutation -

  • can have genetic origin in the absence of a family history of the disorder
  • one explanation is mutation in parental DNA which can be caused by radiation, poison or viral infection
  • evidence for mutation comes from positive correlations between paternal age (increased risk of sperm mutation) and risk of schizophrenia - increasing from around 0.7% with father under 25 to over 2% in fathers over 50
• neural correlates of schizophrenia -

  • brain function or structure
  • neurotransmitter dopamine - important in functioning of several brain systems related to the symptoms of schizophrenia
• original dopamine hypothesis -

  • based on discovery that drugs used to treat schizophrenia (antipsychotics which reduce dopamine) caused symptoms similar to those in people with Parkinson's disease - condition associates with low dopamine levels
  • therefore schizophrenia might be result of high levels of DA in subcortical areas of the brain
  • eg excess of DA receptors in pathways from subcortex to Broca's area (speech production) may explain symptoms such as poverty of speech or auditory hallucinations
• updated versions of dopamine hypothesis -

  • Davis et al (1991) proposed addition of abnormally low DA in brains cortex (hypodopaminergia) - explain symptoms
  • eg low DA in brains prefrontal cortex (responsible for thinking) could explain cognitive problems (negative symptoms)
  • suggested cortical hypodopaminergia leads to subcortical hyperdopaminergia
  • also try to explain origins of abnormal DA function - genetic variations and early experiences of stress make people more sensitive to cortical hypodopaninergia and hence hyperdopaminergia