Biological explanations of Schizophrenia

Question 1

What are the different areas that can be discussed

Answer 1

• genetic basis
• neural corralates
• original DA hypothesis
• updated DA hypothesis

Question 2

What aspects make up genetic basis

Answer 2

• family studies
• candidate genes
• mutation

Question 3

What is the research for the genetic basis

Answer 3

• Family studies - Gottesman 1991
• Finnish adoption study - Tiernari 1991
• candidate genes - Ripke et al 2014
• mutation - brown et al 2002

Question 4

what research is there for neural correlates

Answer 4

• brain structure - Juckel et al 2006

Question 5

Give research for the dopamine hypothesis

Answer 5

Researchers aren’t famous studies so names aren’t important.

Question 6

Outline Gottesman 1991 findings

Answer 6

Gottesman conducted twin studies which had a concordance rate of 17% between DZ twins and 48% between MZ twins. This shows strong evidence that genetics are an important cause of SZ

monozygotic and dizygotic

Question 7

Evaluate Gottesman 1991

Answer 7

• The problem with twin studies is that concordance rates are never 100%. This suggests that genetics are not the only factors.
  e.g. hostile family relationships or environmental factors or drug abuse are important.
• Another weakness is that MZ twins are rare and only 1% of them would be expected to have SZ. Therefore we must be cautious when drawing conclusions.
• Another weakness is that twins share an environment so it is difficult to determine what is due to genetics.

Question 8

Outline Tienari 1991

Answer 8

Tienari 1991 was a Finnish adoption study which consisted of 2 groups.
group 1 - had 155 adopted children whose biological mother had SZ
group 2 - consisted of a matched group of adoptibe children with no family history of SZ.

Question 9

Outline Tienari 1991 findings and conclusion

Answer 9

In group 1: 10% of children developed SZ.
In group 2: 1% of children developed SZ
This is strong evidence to suggest that genetics are important, but not a complete explination of the cause of SZ.

Question 10

Describe what is meant by neural correlates

Answer 10

Neural correlates are patterns of structure or activity in the brain that occur in conjunction with an experience such as SZ and may be implicated in its origins. Both positive and negative symptoms have neural correlates.

Question 11

Give an example of neural correlates of negative symptoms

Answer 11

avolition: loss of motivation → motivation involves anticipation of a reward → certain regions of the brain are associated with this e.g. ventral striatum. Therefore it follows that an abnormality of areas such as the ventral striatum may be involved in the development of avolition.

Question 12

Give research to support neural correlates of negative symptoms

Answer 12

Juckel et al 2006
observed a negative correlation between activity levels in the ventral striatum and the severity of negative symptoms of SZ.

Question 13

What is dopamine

Answer 13

dopamine is a neurotransmitter, associated with attention and motivation

Question 14

Outline the original DA hypothesis

Answer 14

SZ has been linked to excess activity of dopamine in subcortical areas of the brain.
(Hyperdopaminergia)

Question 15

Explain the original DA hypothesis

Answer 15

• High DA activity in subcortex associated with hallucinations and speech poverty.
• There is an excess of DA receptors in pathways linking subcortex to Broca’s area.
• May explain specific symptoms e.g. speech poverty / auditory hallucinations.

Question 16

Suggest the causes for the original DA hypothesis

Answer 16

• Elevated pre synaptic dopamine (more is being synthesised and stored in the vesicles of the pre-synaptic neuron)
• Excess dopamine released into the synapse
• Increased density of receptors on the post-synaptic neuron

Question 17

briefly outline the updated DA hypothesis

Answer 17

SZ has also been linked to low activity of dopamine in the prefrontal cortex. (hypodopaminergia)

Question 18

Explain the updated DA hypothesis

Answer 18

Dopamine neurons help guide attention, so disturbances may lead to problems with perception, attention and thought, all characteristics of SZ.
This imbalance could be inherited or due to environmental factors (e.g. drug use).

Question 19

suggest how the updated DA hypothesis could explain symptoms of SZ

Answer 19

• Low levels of dopamine in the prefrontal cortex (responsible for thinking), could explain negative symptoms.
• Genetics and early experiences of stress make some people more senstive to cortical hypodopaminergia.

Question 20

Give evidence to support the original DA hypothesis

Answer 20

Antipsychotic drugs:
- Antipsychotic drugs, which block the activity of dopamine in the brain, have reduced positive symptoms of SZ (e.g. hallucinations). This suggests that dopamine overactivity is important in SZ

Question 21

Give evidence to support the updated DA hypothesis

Answer 21

Not all patients with SZ benefit from dopamine antagonist drugs.
- Clozapine is a very effective treatment for SZ, binding to dopamine and serotonin receptors. This suggests that dopamine over-activity is not the only cause of SZ.

Question 22

Which three mechanisms does the orignial DA hypothesis suggest may be responsible fot hyperdopaminergia

Answer 22

• Elevated pre synaptic dopamine (more is being synthesised and stored in the vesicles of the pre-synaptic neuron)
• Excess dopamine released into the synapse
• Increased density of receptors on the post-synaptic neuron

Question 23

Give a strength of the biological explanation

Answer 23

A strength is that there is research support from Gottesman and Tienari. This is a strength because it shows that genetics plays an important role in SZ. This shows that some people are more vunerable to SZ as a result of their genetic make-up.

Question 24

outline Ripke et al 2014

Answer 24

combined all previous data from genome-wide studies of SZ. He found that 108 seperate genetic variations were associated with slightly increased risk of SZ.

Question 25

Outline Brown et al 2002

Answer 25

Found evidence for mutation comes from a positive correlation between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia.