BE AO1

• family studies 


  Gottesman et al

  • MZ twins have a 47% concordance rate
  • DZ twins have a 17%
  • grandchildren = 5%
  • siblings = 9%
• schizophrenia is polygenetic and aetiorogically heterogenous, each individual gene induces a small increased risk, different combinations can lead to schizophrenia
• Ripke et al


  37,000 patients, 108 separate genetic variations associated with an increased risk
• original dopamine hypothesis


  positive symptoms are caused by an excess of dopamine in the subcortex

  this causes the neurone that respond to dopamine too fire too often and transmit too many messages - the message overload produces the positive symptoms
• revised dopamine hypothesis - Davis and Khan


  negative and cognitive symptoms arise from a deficit low levels of dopamine in the prefrontal cortex
• Johnstone et al


  early research focused on sz having enlarged ventricles associated with damage to central brain areas and the prefrontal cortex which has been associated with negative symptoms
• Ho et al


  structural brain damage often evident as first onset of sz, MRI scans 3 years later and found damaged areas got worse over time especially frontal lobes which increase the severity of symptoms
• neural correlates


  ventral striatum is involved in anticipation of reward. loss of motivation in sz may be expressed by low activity levels
• Jackel et al


  negative correlation between ventral striatum activity and overall negative symptoms
• Allen et al


  patients experiencing auditory hallucinations recorde lower levels superior temporal gyrus and anterior cingulate gyrus