Biological explanations for schizophrenia

Question 1

Gottesman (1991)

Answer 1

• Identical twins share 100% of their genes and 50% with parents or siblings
• a strong relationship between the degree of genetic similarity and shared risk of schizophrenia is demonstrated by studies such as Gottesman’s
• this was a large-scale family study which showed a risk of 48% risk of identical twins both developing schizophrenia
• this is compared to a 17% risk between fraternal twins

Question 2

Candidate genes for schizophrenia

Answer 2

• schizophrenia is polygenic since there a number of genes which increase the risk of developing schizophrenia a small amount
• schizophrenia is etiologically heterogeneous, which means that different combines of factors lead to the condition
  Ripke et al. (2014) looked at lots of data from genome-wide studies of schizophrenia
• he compared 37,000 patients to 113,000 controls and concluded that there were 108 genetic variations which increased risk of schizophrenia

Question 3

Dopamine hypothesis

Answer 3

• chemical messengers seem to work differently from normal in the brain of a schizophrenic
• in particular, this applied to dopamine, which is important for the functioning of several brain systems

Hyperdopaminergia

• high levels or activity of dopamine in the sub-cortex
• the original dopamine hypothesis focusses not the role of this on schizophrenia
• for example, an excess of dopamine receptors in Broca’s area, which is responsible for speech production, may be linked to poverty of speech of auditory hallucinations

Hypodopaminergia

• investigated by Goldman-Rakic et al. (2004)
• the role of low levels of dopamine in the prefrontal cortex, which is responsible for thinking and decision making
• and how it links to negative symptoms of schizophrenia
• both the explanations may be correct, with high levels of dopamine in some brain areas and low levels in others

Question 4

Neural correlates

Answer 4

• neural correlates are measurements of the structure or functions of the brain correlating to an experience
• negative and positive symptoms have neural correlates
• loss of motivation is linked to avolition, a negative symptom of sz, and motivation involves anticipation of rewards
• a number of regions within the brain, such as the ventral striatum, are involved in anticipation, suggesting that an abnormality in these areas is involved in the development of avolition

Question 5

Positive and negative neural correlates

Answer 5

Juckel et al. (2006)

• found lower levels of brain activity when it was measured in the ventral striatum of schizophrenia patients in comparison to the control group
• negative correlation was seen between activity levels in ventral striatum and severity of negative symptoms
• suggests that activity in ventral striatum is a neural correlate of negative symptoms of schizophrenia

Allen et al. (2007)

• scanned the brains of participants who were experiencing auditory hallucinations
• he compared them to a control group
• both groups were tasked with listening to pre-recored speech and identifying it as their own or someone else’s
• lower activation levels were found in the superior temporal gyrus and the anterior cingulate gyrus in the schizophrenia group
• the group also made more errors overall in the task then the control group
• we can therefore say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination

Question 6

(+) EVAL - multiple sources of evidence for genetic susceptibility

Answer 6

• there is a lot of strong evidence which supports the idea of genetic vulnerability to schizophrenia
• Gottesman (1991) demonstrates how genetic similarity and shared risk of schizophrenia are linked
• Tienari et al. (2004) as well as other adoption studies show that children of sz sufferers are still at a heightened risk of developing the disorder if adopted into a family without the disorder
• Ripke et al. (2014) provides evidence which shows that particular genetic variations significantly increase schizophrenia risk

Question 7

(-) EVAL - mixed evidence for the dopamine hypothesis

Answer 7

• Curran et al. (2004) showed that dopamine agonists, e.g. amphetamines which increase level of dopamine can make schizophrenia worse and produce schizophrenia-like symptoms in non-sufferer
• antipsychotic drugs work by reducing dopamine activity
• both of these drugs show that dopamine has an important role in schizophrenia
• Lindstroem et al. (1999) found that chemicals needed to produce dopamine are taken up quicker in the brain of a sz sufferer than a control
• this suggests greater production of dopamine in schizophrenics
• there is also some evidence to suggest that dopamine does not provide a full explanation
• Ripke et al. (2014) identified 108 candidate genes which played a role in schizophrenia risk
• Moghaddam and Javitt (2012) focussed on glutamate, another neurotransmitter
• therefore, evidence for the dopamine hypothesis is limited

Question 8

(-) EVAL - correlation-causation problem

Answer 8

• one of the main issues with neural correlates and how relate to schizophrenia is correlation/causation
• whether the unusual activity in the brain region causes the symptoms or is caused by it
• as for the ventral striatum and negative symptoms, it may be explained by something being wrong in the ventral striatum causing the symptom, or it could be that the negative symptoms mean that less info is passed through the ventral striatum, thus a reduction in activity
• there may, as an alternative, be a third factor which influences the negative symptoms and ventral striatum