Biological Explanations for Schizophrenia

?

Genetic Basis of Sz

Sz runs in families

  • Weak evidence for a genetic link as family members share aspects of their environment
  • As genetic similarity increases, so does the probability of sharing Sz - investigated by Gottesman
  • If one Mz twin has Sz, there is a 48% chance of the other twin developing Sz
  • If one Dz twin has Sz, there is a 17% chance of the other twin developing Sz

Candidate genes

  • Individual genes are associated with risk of inheritance as a number of genes increase the risk of Sz, so it appears to be polygenic - needs a number of factors to work in combination
  • Appears to be aetiologically heterogeneous - different combinations of factors lead to the same condition
  • Genes associated with increased risk include those used in coding for the functioning of neurotransmitters including dopamine (DA)
1 of 5

Dopamine Hypothesis

Neurotransmitter involved in excitatory effect and pleasure. High levels associated with Sz, low levels associated with Parkinson's.

DA 1: Hyperdopaminergia  High levels of DA in the subcortex. Excess of DA receptors in Broca's area - responsible for speech production - may be associated with speech poverty and/or audio hallucinations.

DA 2: Hypodopaminergia  Focus on abnormal DA systems in the brain's cortex. Low levels of DA in the prefrontal cortex - responsible for decision making and thinking - associated with the negative symptoms of Sz.

It is possible that both explanations are correct.

2 of 5

Neural Correlates

The structure or function of the brain. Both positive and negative symptoms have neural correlates.

Positive symptoms: Brains of patients experiencing auditory hallucinations were compared to control group whilst they identified recorded speech as their own or others. Lower activity in gyrus and more mistakes in hallucination group than control group. Reduced activity in this area of the brain is a neural correlate of auditory hallucinations.  

Negative symptoms: Avolition is the loss of motivation. Part of motivation is the anticipation for a reward. The ventral striatum area of the brain is involved in this anticipation so could also be involved in the development of avolition. It has been found that those with Sz have lower activity levels in the ventral straitum than control groups. Also a negative correlation between ventral straitum activity levels and severity of negative symtoms. Activity in the ventral straitum is a neural correlate of negative symptoms.

3 of 5

Strong Evidence for Genetic Susceptibility

  • Gottesman study shows how genetic similarity and Sz are related
  • Adoption studies, e.g. Tienari, show children of Sz sufferers are still at greater risk of developing Sz even if adopted into families with no history of Sz
  • Studies conducted at molecular level, e.g. Ripke, show that particular genetic variations increase the risk of Sz - 108 separate genetic variations associated with increased risk of Sz
  • Overwhelming evidence that certain genetic factors make people more vulnerable to developing Sz
  • Not completely genetic basis
  • Number of factors in the environment involved - If Sz was completely genetic then concordance rates would be 100%; they are 48%
4 of 5

Mixed Evidence for Dopamine Hypothesis

  • Dopamine agonists, e.g. amphetamines, increase DA levels and make of Sz worse and produce Sz-like symptoms. Antipsychotics reduce DA levels. Both drugs support role of DA in Sz
  • Radioactive labelling studies, e.g. Lindstroem, found that chemicals needed to produce DA are taken up quicker in those with Sz than controls, so they need to produce more DA as a result
  • Evidence shows that DA does not provide a complete explanation for Sz
  • Ripke found that although DA plays a key role, other neurotransmitters do too, such as serotonin and glutamate

Evidence for DA hypothesis is mixed

5 of 5

Comments

No comments have yet been made

Similar Psychology resources:

See all Psychology resources »See all Schizophrenia resources »