Biological Explanations of SZ

• Genetic Explanations


  Gottesman - greater genetic similarity amongst family members is associate with how likely it is to develop SZ.

  many candidate genes

  Aetiologically Heterogenous - different studies have found different candidate genes, suggesting different combinations - SZ

  Polygenic - needs several factors to work together to develop SZ

  Ripke et al - combined all previous data from genome studies. genetic makeup of 37,000 patients compared to 113,000 controls.

  found 108 genetic variations associated with increased risk of SZ. associated genes linked with function of several NTs, including dopamine.
• Evaluation - Genetic explanation

  Gottesman showed genetic similarity and share risk of SZ are closely related

  adoption studies by Tienari et al showed children of SZ were still at heightened risk of developing SZ even when adopted into families with no history of condition.

  supports idea genetic factors make some people more vulnerable to SZ and genetics play a key role in development of disorder
• Dopamine Hypothesis


  SZ may result from excess levels of dopamine (Seidman).

  different view is neurones in brains of SZ patients are oversensitive to dopamine -> producing an exaggerates response and relay unnecessary messages to brain (more APs fired)

  Hyperdopaminergia in sub-cortex

  - high levels of dopamine in sub-cortex

  - e.g. an excess of dopamine receptors in Brocas areas may be responsible for speech poverty and auditory hallucinations.

  Hypodopaminergia in cortex

  - more recent theories have looked at abnormal dopamine systems in cortex

  - Goldman-Rakic have identified a role for low levels of dopamine in pre-frontal cortex (decision making + thinking) in the negative symptoms of SZ.
• Evaluation - Dopamine Hypothesis

  e.g. dopamine agonists like amphetamines, which increase levels of dopamine can make SZ symptoms worse or produce SZ-like symptoms in non-sufferers (Curran et al)

  Antipsychotics work by reducing dopamine activity (Tauscher et al)

  however, there's evidence that dopamine doesn't provide the full picture. Ripke et al study showed SZ candidate genes code for other neurotransmitters, suggesting there may be other NTs e.g. glutamate, involves in development of SZ.
• Neural Correlates


  measurements of structure and function of the brain that correlate with an experience (SZ)

  Positive symptoms - Allen et al

  - scanned brains of patients with auditory hallucinations and compared them to control group whilst identifying pre-recorded speech as belonging to themself or others.

  - lower activity in superior temporal gyrus and anterior cingulate gyrus were found in hallucination group, who also made more error than control group.

  Negative symptoms

  - avolition - motivation comes from anticipation of rewards, which invovles ventral striatum in brain. abnormality could be associated with avolition.

  - Juckel et al measured activity in ventral striatum in SZ and found lower level of activity than controls. saw a negative correlation between activity in region and severity of negative symptoms
• Evaluation - Neural Correlates

  a number of neural correlates of SZ symptoms, both positive and negative and evidence abnormally functioning and evidence that abnormally functioning brain systems may be involved, there's still issue of causation.

  hard to know whether unusual brain activity is the cause or an effect of SZ.

  e.g. there's a correlation between activity in ventral striatum and negative symptoms. we can't know if it's reduced activity that cause negative symptoms of whether negative symptoms cause less info to pass through ventral striatum, resulting in reduced activity.

  Alternatively there could be a 3rd variable affecting both negative symptoms and ventral striatum activity. results in the existence of neural correlates in SZ actually tells us little about the cause of the disorder.