Schizophrenia: Biological explanation

Question 1

What are the 3 genetic basis for SZ? (AO1)

Answer 1

• Family studies
• Candidate genes
• The role of mutation

Question 2

Explain family studies as a genetic basis for SZ:

Answer 2

• Family studies have confirmed that the risk of SZ increases in line with genetic similarity to a relative with the disorder.
• Gottesman completed a large scale family study. Found that if a relative has been diagnosed with SZ, you have a 9% chance of also developing it if the individual is your sibling, and 48% chance if they are your identical twin.
• Family members tend to share the same environment as well as many of heir genes, so the correlation represents both- with family studies still providing good supporting evidence.

Question 3

Explain candidate genes as a genetic basis for SZ:

Answer 3

• Early research looked for a single genetic variation in the belief that one faulty gene could explain SZ.
• Current research shows that it is most likely a number of different genes that are involved e.g. SZ is polygenic.
• The most likely genes would be those coding for neurotransmitters e.g. dopamine.
• Ripke combined all previous data from genome-wide SZ studies, comparing the genome of those with SZ and those without.
• 108 different genetic variations were associated with having a slightly increased risk of SZ.
• Because studies have identified different candiate genes, suggests that SZ aetiologically heterogeneous .

Question 4

Explain the role of mutation as a genetic basis for SZ:

Answer 4

• SZ can also have a genetic origin in the absence of a family history of the disorder.
• One explanation for this is a mutation in the parental DNA e.g. due to radiation, diet.
• Evidence for mutations comes from positive correlations between paternal age (associated with an increased risk of sperm mutation) and the risk of SZ, increasing from around 0.7% in fathers under 25, and to 2% in fathers over 50.

Question 5

What are the 2 neural correlates for SZ?

Answer 5

• The original dopamine hypothesis
• Updated versions of the dopamine hypothesis

Question 6

Explain the original dopamine hypothesis as a neural correlate for SZ:

Answer 6

• The original hypothesis was based on the discovery that drugs used to treat SZ (antipsychotics, which inhibit dopamine production) caused simptoms similar to those in people with Parkinson’s disease, a condition associated with low dopamine levels.
• Suggests that SZ may be due to high levels of dopamine in subcortical areas of the brain.
• E.g. excess dopamine receptors in pathways from the subcortex to the Broca’s area (responsible for speech production) may explain specific symptoms of SZ, such as speech poverty.

Question 7

Explain the updated versions of the dopamine hypothesis as a neural correlate for SZ:

Answer 7

• Davis proposed the idea of abnormally low dopamine levels in the brain’s cortex.
• This can too explain symptoms of SZ- e.g. low dopamine levels in the prefrontal cortex (responsible for thinking) could explain cognitive problems, such as negative symptoms of SZ.
• Current versions of the dopamine hypothesis try to explain the origins of abnormal dopamine activity. It is suggested that both genetic variations and early experiences of stress contribute to the development of SZ e.g. through predispositions and physiological stress.

Question 8

What are the three evaluation points for the genetic basis for SZ:

Answer 8

1) Research support (S)
2) Environmental factors (L)
3) Genetic counselling (L)

Question 9

Explain research support (S) as an evaluation point for the genetic basis for SZ:

Answer 9

• A strength is that there is a strong evidence base.
• Family studies such as Gottesman show that risk increases with genetic similarity to a family member with SZ.
• Adoption studies show that biological children of parents with SZ are at a heightened risk even if they grow up with an adopted family
• Research from Hilker showed a concordance rate of 33% for identical twins, and 7% for non-identical twins when placed in an adoptive scenario.
• Shows that some people are more vulnerable to developing SZ due to their genetic make-up.

Question 10

Explain environmental factors (L) as an evaluation point for the genetic basis for SZ:

Answer 10

• A limitation is that there is clear evidence to show that environmental factors also increase the risk of developing SZ.
• These environmental factors include both physical and osychologival influences. Biological influences include birth complications, and smoking cannabis during adolescence.
• Psychological risk factors include childhood trauma which leaves people more vulnerable to developing mental health issues in adulthood.
• Morkved found that 67% of people with SZ and related psychotic disorders reported at least one childhood trauma opposed to 38% of a match group without any psychotic disorders,
• Suggests that genetic factors alone cannot provide a complete explanation for SZ.

Question 11

Explain genetic counselling (L) as an evaluation point for the genetic basis for SZ:

Answer 11

• A benefit of research into SZ is that it can help parents make informed decisions abut whether to have children who risk having a poor quality of life if they develop SZ.
• HOWEVER, the risk provided by genetic counselling is just an average figure across the whole population.
• It will not actually reflect the probability of a child developing SZ because any given child will experience a particular environment which also exposes them to risk factors.
• E.g. a child’s probability of developing SZ will be much higher than suggested by their genetic probability if they experience a childhood trauma and smoke cannabis during adolescence.

Question 12

What are the 3 evaluation points for the neural correlates for SZ?

Answer 12

1) Evidence for dopamine (S)
2) Amphetamine psychosis (S)
3) Glutamate (L)

Question 13

Explain evidence for dopamine (S) as an evaluation point for the neural correlates for SZ:

Answer 13

• A strength is that there is support for the idea that dopamine is involved in SZ.
• Amphetamines increase dopamine activity and worsen symptoms in those with SZ, and induce symptoms in those without.
• Antipsychoitc drugs reduce dopamine activty and also reduce the intensity of symptoms.
• Some candidate genes act on the production of dopamine or dopamine receptors.
• Strongly suggests that dopamine is involved in the symptoms of SZ.

Question 14

Explain glutamate (L) as an evaluation point for the neural correlates for SZ:

Answer 14

• A limitation of the dopamine hypothesis is the evidence of the role of glutamate.
• Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with SZ.
• Also, several candidate genes for SZ are believed to be involved in glutamate production or processing.
• Suggests that other neurotransmitters must have a central role in SZ.

Question 15

Explain amphetamine use (S) as an evaluation point for the neural correlates for SZ:

Answer 15

• A strength is that the link between amphetamine use and SZ symptoms supports the dopamine hypothesis.
• Tenn induced SZ-like symptoms in rats using amphetamines and then relived these symptoms using drugs that decrease dopamine activity
• In other research amphetamines have been found to raise dopamine levels so there is evidence of a link between amphetamine use and SZ symptoms.
• Suggests that it is increased dopamine levels that mimic the symptoms of SZ.