Biological Explanations of Schizophrenia

What are the 3 parts of the biological explanations of Sz?

- the genetic basis of schizophrenia

- the dopamine hypothesis

- neural correlates of schizophrenia

What are the 2 parts of the genetic basis of Sz?

- Sz runs in families

- candidate genes

Summarise how Sz runs in families

- there's quite weak evidence in itself for a genetic link as family members tend to share the same environment as well

- there's been systematic investigations of the extent to which greater genetic similarity between family members is associated with the likelihood of both developing schizophrenia

- there's a strong relationship between the degree of genetic similarity and shared risk of Sz shown by findings from Gottesman's large scale family study

What are some of Gottesman's findings?

- half siblings have more than half the risk of full siblings

- the greater the genetic similarity the greater the risk

- 6% of parents develop Sz after children develop it

- DZ twins have a higher risk than siblings despite sharing the same no. of genes

Summarise how candidate genes may lead to Sz development

- Sz is polygenic meaning multiple genes are linked to Sz

- because a number of studies have identified different genes this also suggests Sz is aetiologically heterogeneous

- Ripke et al carried out a large scale study combining data from genome-wide studies and found 108 genetic variations in the Sz sample of 37,000 compared with 113,000 controls

What does aetiologically heterogeneous mean?

Different combinations of factors can lead to the condition

What is hypodopaminergia?

Under stimulation of the reward system

What can hypodopaminergia lead to?

- Sz sufferer is unmotivated by behaviours which would previously have led to feelings of pleasure

- manifested in negative symptoms e.g avolition

- affects patient's ability to communicate effectively as low levels will impact speech production

What is hyperdopaminergia?

Over stimulation of reward system

What can hyperdopaminergia lead to?

- correlates highly with positive symptoms

- patient experiences sensory hallucinations which they can't distinguish between reality and falsehood

- patients struggle with focus and inability to concentrate

What are neural correlates?

measurements of the structure or function of the brain that correlate with an experience

Summarise neural correlates of negative symptoms

- avolition is the loss of motivation, motivation involves anticipation of reward

- Juckel et al (2006) measured activity levels in the ventral striatum and found lower levels of activity in Sz sufferers than in controls

- there was a negative correlation shown between activity in the ventral striatum and severity of negative symptoms

Summarise neural correlates of positive symptoms

- Allen et al (2007) compared Sz sufferers who were experiencing auditory hallucinations with a control group

- they gave pps the task of identifying whether pre-recorded speech was that of their own or others

- they simultaneously scanned pps brains

- the experimental group showed lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus

What is the superior temporal gyrus?

A critical brain region in the temporal lobe responsible for auditory processing, language comprehension, and social cognition

What is the anterior cingulate gyrus?

The anterior cingulate gyrus is involved in regulating autonomic processes in the body.

It detects when competing stimuli create conflict, signalling a higher chance of error

How does detracting from the role of genes weaken Gottesman's findings?

- for example it states that MZ twins only had a concordance rate of 48% even though they share 100% of genes, and children of schizophrenic parents had a much lower risk of developing Sz

- this is a problem as if Sz were entirely genetic, we would expect a 100% concordance

- the fact that more than half of identical twins do not develop Sz suggests that genes alone aren't sufficient and environmental factors must play a role

- therefore indicating that Sz isn't purely genetically determined supporting the diathesis-stress model

How does Tienari (2004) add support for the genetic explanation of Sz?

- she found that 155 adopted children born to Sz mothers had a concordance of 10% compared to 1% in adopted children without Sz mothers

- this shows that despite being raised in non-schizophrenic adoptive families, the risk was greater for those whose biological mother had Sz

- it also shows that adoption isn't a complete protective factor as removing the children from a high risk Sz environment doesn't eliminate the risk entirely

- this doesn't only add support to the genetic explanation of Sz, but also provides suggestions to improve the risk of those who are genetically vulnerable by placing them in homes where there's no risk of Sz (risk reduced from 13% to 10%)

How does a lot of evidence support the dopamine hypothesis of Sz?

- research has shown that drugs that increase levels of dopamine also produce psychotic symptoms meaning dopamine is somehow implicates in positive symptoms of Sz, supporting the hyperdopaminergia hypothesis

- an excess number of dopamine receptors have been found in Broca's area which is linked to speech production, which can help to explain disorganised speech and auditory hallucinations as overstimulation of Broca's area by dopamine can cause overactivity

How can issues with causality weaken the dopamine hypothesis of Sz?

- it is difficult to assess brain levels of dopamine in schizophrenics meaning there may be issues of causality when trying to understand its role in the illness

- high levels of dopamine could actually be a symptom of Sz rather than a cause, suggesting it may actually be another, unknown, 3rd factor which caused Sz to occur

- Clozapine is the most effective drug at reducing schizophrenic symptoms

- it acts on serotonin as well as dopamine meaning that serotonin must also be involved in Sz - not just dopamine

- therefore meaning the dopamine hypothesis is not a complete explanation

- this inconsistency in evidence means our understanding of the role of dopamine in the development of Sz is inconclusive making it difficult to accept this as a sole explanation