A01: Biological Explanations for Schizophrenia

• Biological Explanations for Schizophrenia:

  • Genetic
  • Neural
• The Genetic Basis of Schizophrenia:

  Genes:

  • Candidate Genes
  • Family Studies
  • Mutation
• Booklet Biological Explanations

  Genetics

  • Family Studies
  • Candidate Genes / Genes
  • Mutations

  Neural Correlates

  • Dopamine Hypothesis
  • Neural correlates of +ve symptoms
  • Neural correlates of -ve symptoms
• Neural Correlates

  Neural correlates are measurements which look at the structure of the brain which are correlated with particular schizophrenic experiences to see if there is a pattern

  • Neural correlates include but are not limited to dopamine levels. There are other neural correlates which link to the symptoms of sz

  Neural correlates of positive symptoms

  Neural correlates of negative symptoms

  Parts of the brain
• Genetic Explanations: Family Studies:

  Strong relationship between degree of genetic similarity & shared risk of schizophrenia.

  • Gottesman's (1991) large-scale study looking at genetic similarity & likelihood of developing sz:
  • found someone with SZ aunt has 2% chance of developing it, 9% for sibling & 45% for identical twin
  • Family members also share env but still indicates support for genetic view.

  A) ?

  
• (SIBILINGS)Genetic Explanations: Family Studies: P2

  • More genetic similarity more risk
  • MZ share 100% genes, highest risk (48%) - not 100% show env factors influence sz
  • DZ are sibilings but higher risk vs siblings despite sharing same n.o of genes coz more similar env factors/identity issues
  • Half siblings (6%) more than half risk of full siblings (9%) (expect them to have 1/2 risk of siblings (4.5%) but half higher risk then expected coz divorce, parent died, traumatic event etc

  A) ?

  
• PART 3 (PARENTS)Genetic Explanations: Family Studies: P2

  • Parent high risk if kid has sz coz genetic predisposition (no sz) that not triggered. Looking after kid with sz may trigger parent sz (env stressors) (6% )
  • If u have sz, kid has 13% chance

  A) ?

  
• Types of Twins

  DZ - Fraternal Twins - Non Identical Twins (dizygotic twins)

  MZ - Identical Twins (monozygotic twins)
• GE: Candidate Genes: P1

  Early research looked unsuccessfully for a single genetic variation to explain SZ.

  • Candidate Genes: Specific genes which may be associated with risk of inheritance. There have been a n.o identified which each confer small increased risk of SZ. But as no single gene, suggest SZ is POLYGENIC: means it requires several genes to work in combination for Sz
  • Number of studies identified different genes also suggests Sz is aetiologically heterogeneous: means different combinations of factors can lead to condition (risk affected by different combinations).
• GE: Candidate Genes: P2

  • Ripke et al (2014) combined previous data from genome-wide studies in large scale study (those studies looking at whole human genome not particular genes).
  • Found 108 separate genes (genetic variations) in Sz sample of 37,000 (compared with 113,000 controls) associated with slightly increased risk of SZ.
• Genetic Explanations: Mutation:

  • SZ can also have a genetic origin in the absence of a family history because of mutation in parental DNA.
  • Evidence comes from the correlation between paternal age (associated with increased risk of sperm mutation) and risk of SZ (Brown et al 2002)
• The Neural Basis of Schizophrenia:

  • Neural Correlates:

  Dopamine Hypothesis

  Neural Correlates +ve & -ve symptoms
• Neural Correlates: Dopamine Hypothesis

  Dopamine (DA) is widely believed to be involved in SZ coz it is featured in the functioning brain systems related to the symptoms of SZ.

  • HypErdopaminergia
  • HypOdopaminergia
• Neural Correlates: Dopamine Hypothesis: Hyperdopaminergia

  Original DA Hypothesis

  Hyperdopaminergia linked to subcortex

  • High levels of dopamine (receptors) activity in subcortex (central areas of the brain) associated with (auditory) hallucinations & speech poverty
  • Dopamine responsible for perception, so high levels lead to “over-perceiving” your env (hallucinations).
  • Excess of DA receptors in pathways linking subcortex pathways to Broca's area - explain auditory hallucinations & disordered thinking.
• Neural Correlates: Dopamine Hypothesis: Hypodopaminergia

  Low levels of dopamine in prefrontal cortex lead to -ve symptoms. 

  • Updated/newer version
  • Low levels in prefrontal cortex lead to blocked thoughts (alogia), limited emotional range (affective flattening), poor decision making (avolition). Prefrontal cortex (responsible for thinking) explain -ve symptoms.
  • Explains origins of abnormal DA - genetic variations & early experiences of stress make people more sensitive to cortical hypodopaminergia & hence subcortical hyperdopaminergia (howes et al)
• Neural Correlates/explanations

  Neural correlates are measurements which look at structure of brain which are correlated with particular schizophrenic experiences to see if there is a pattern

  • Neural correlates include but not limited to DOPAMINE LEVELS.
  • There are other neural correlates which link to the symptoms of sz:

  Neural correlates of positive symptoms

  Neural correlates of negative symptoms

  Parts of the brain
• Neural correlates of +ve symptoms

  Allen et al (2007) compare Sz sufferers experiencing auditory hallucinations vs control group

  • Pps identify if pre-recorded speech was own or others. Simultaneously scan pps brains. Experimental group: lower activation levels in superior temporal gyrus (contain primary auditory cortex responsible for processing sounds) & anterior cingulate gyrus (key for controlling other brain areas when processing stimuli)

  Show 2 areas are neural correlates of +ve symptoms. Explain auditory hallucinations as inability to recognise internal monologue being self generated
• Neural Correlates of -ve symptoms:


  Avolition is loss of motivation. Motivation involves anticipation of reward.

  • Juckel et al (2006) measured activity levels in ventral striatum (area of brain involved in reward anticipation), found lower levels of activity in Sz sufferers vs control. There -ve correlation between activity in VS & severity of -ve symptoms .

  Suggests that VS is a neural correlate of -ve symptoms. If activity levels in VS are low then anticipation of a reward not present. If there no anticipation of a reward, there no reason to engage in behaviours to bring about reward.